5^th World Congress on Neurology and Therapeutics March 14-16, 2016 London, UK

Biography:

Abstract:

Background: Single intrahippocampal (IH) injection of amyloid beta (Aβ (1-42)) in rats causes mitochondrial dysfunction, oxidative stress, glial cell activation, and apoptosis hence results in cognitive dysfunction. Thus, the study was designed to evaluate the neuroprotective effect of coenzyme Q10 (CoQ10) and its modulation through minocycline (Mino) against Aβ (1-42) induced cognitive dysfunction and behavioral, biochemical, molecular and histological alterations. Methods: In the present study, Aβ (1-42) (1µg/µl saline) has been administered bilaterally to the hippocampal region of rat brain followed by chronic CoQ10 (20 and 40 mg/kg, i.p.), Mino (50 mg/kg, i.p.) and its combination administration for 21 days. Parameters like body weight and locomotor activity was evaluated weekly and Morris water maze (MWM) was performed in the last week and time spent in target quadrant (TSTQ) on day 21 followed by biochemical (lipid peroxidation, nitrite, catalase, reduced glutathione, catalase, superoxide dismutase, acetylcholinesterase), molecular (TNF-α level) and histopathological (H&E staining) parameters. Results: Single bilateral IH Aβ (1-42) administration results in reduction of body weight, marked motor impairment, impaired cognitive performance (MWM and TSTQ), increased oxidative stress, increased inflammatory cytokines and histopathological alterations. However, chronic treatment with CoQ10 (20 and 40 mg/kg) and Mino (50 mg/kg) treatment significantly attenuated behavioral parameters, acetylcholinesterase level and oxidative damage and TNF-α level and histopathological alterations. Further, combination of CoQ10 (40 mg/kg) with Mino (50 mg/kg) significantly potentiated their protective effect as compared to their effect alone. Conclusion: The present study highlights the involvement of possible microglia modulatory mechanism of CoQ10, minocycline and their combination against IH Aβ (1-42) induced oxidative damage and neuroinflammation.

Biography:

Abstract:

Dietary omega-3 fatty acids have been recognized to improve brain cognitive function. Deficiency leads to dysfunctional zinc metabolism associated with learning and memory impairment. The objective of this study is to explore the effect of short-term dietary omega-3 fatty acids on hippocampus gene expression at the molecular level in relation to spatial recognition memory in mice. A total of 24 male BALB/c mice were randomly divided into four groups and fed a standard pellet as a control group (CTL, n = 6), standard pellet added with 10% (w/w) fish oil (FO, n = 6), 10% (w/w) soybean oil (SO, n = 6) and 10% (w/w) butter (BT, n = 6). After 3 weeks on the treatment diets, spatial-recognition memory was tested on a Y-maze. The hippocampus gene expression was determined using a real-time PCR. The results showed that 3 weeks of dietary omega-3 fatty acid supplementation improved cognitive performance along with the up-regulation of α-synuclein, calmodulin and transthyretin genes expression. In addition, dietary omega-3 fatty acid deficiency increased the level of ZnT3 gene and subsequently reduced cognitive performance in mice. These results indicate that the increased the ZnT3 levels caused by the deficiency of omega-3 fatty acids produced an abnormal zinc metabolism that in turn impaired the brain cognitive performance in mice.

Biography:

Neşe Çelebisoy MD, PhD is a Professor of Neurology, Algology and Clinical Neurophysiology, working in Ege University Medical School Department of Neurology, İzmir and running the Department as Chair since 2014. She is the director of Neuroscience PhD program in Ege University, Institute of Health Sciences. She is primarily involved in neuro-otology, neuro-ophthalmology, headache and electrophysiology. She has sixty-five articles published in journals within the SCI or SCI-expanded and fifty-three articles published in national journals. She is the board member of the Turkish Neurological Society and member of the Turkish Headache Society and Clinical Neurophysiology Society.

Abstract:

Vertigo and headache are frequent symptoms in neurology clinics. After several studies in the field vestibular migraine (VM) has been accepted as the term defining vestibular symptoms that are casually related to migraine and International Headache Society and Barany Society have created a consensus document with diagnostic criteria for this clinical entity. The diagnosis was considered in the appendix of the new International Classification of Headache Disorders (ICHD)-3 beta version of headache classification. VM is the most common cause for recurrent spontaneous vertigo with a lifetime prevalence of 1%, and a one-year prevalence of 0.9% in the general population. It can occur in any period of life. Women are affected more frequently than men with a gender ratio between1.5 and 5. Patients report spontaneous or positional vertigo attacks as well as imbalance. The duration of attacks generally vary from minutes to a few days. Auditory symptoms, including hearing loss, tinnitus and aural pressure have been reported in up to 38% of the patients. However, hearing loss is usually mild and transient. During an attack and in-between attacks the neuro-otological examination is generally normal. Mild central deficits such as persistent positional nystagmus or peripheral deficits such as unilateral caloric hypoexcitability have been reported. The diagnosis mainly depends on history as no abnormalities specific for vestibular migraine can be found by vestibular testing. Therapeutic studies on VM are few and treatment options are mainly based on migraine guidelines.

Biography:

Dr Davide Vito Moretti is consultant neurologist, chief of the clinical neurophysiology service and researcher at the National Institute of Research and Cure for Mental disorders and Dementia S john of God, Brescia, Italy, Professor of neurophysiology at UniLudes University in Lugano. He received his medical degree from Catholic University in Rome and completed his residency in neurology and fellowship in movement disorders at University of Trieste, Italy. Moreover, he received the PhD in neurophysiology at La Sapienza University. Dr Moretti is currently involved in research and care of subjects with Alzheimer's disease and movement disorders in the Alzheimer Operative Unit of the S. John of God Institute.

Abstract:

Recent studies demonstrate that the alpha3/alpha2 power ratio correlates with cortical atrophy, regional hypoperfusion, and memory impairment in subjects with mild cognitive impairment (MCI).METHODS: Evidences were reviewed in subjects with MCI, who underwent EEG recording, magnetic resonance imaging (MRI) scans, and memory evaluation. Alpha3/alpha2 power ratio (alpha2 8.9-10.9 Hz range; alpha3 10.9-12.9 Hz range), cortical thickness, linear EEG coherence, and memory impairment have been evaluated in a large group of 74 patients. A subset of 27 subjects within the same group also underwent single photon emission computed tomography (SPECT) evaluation and a subset of 23 patients underwent positron emission tomography with fluorodeoxydglucose (PET-FDG) analysis. RESULTS: In MCI subjects with higher EEG upper/low alpha power ratio, a greater temporo-parietal and hippocampal atrophy was found as well as a decrease in regional blood perfusion, glucose metabolism and memory impairment.CONCLUSION: The increase of alpha3/alpha2 power ratio is a promising novel biomarker in identifying MCI subjects at risk for Alzheimer's disease

Biography:

Dr Meguid holds her Ph.D. from Alexandria University. She is a professor of human genetics at the National Research Center (NRC) in Egypt. She is a Senior Geneticist at the Genetics Institute, California and Yale University; a fellow of Uppsala University, Sweden. She was selected to win the outstanding L’Oreal UNESCO Award for women in Science for Africa & Middle East (2002). She was given the National Award for Scientific Excellence in Advanced Technology in 2009. NRC Appreciation Prize in Medical Sciences, 2011.She is the Founder of Autistic disorders Clinic in the NRC. She is the head of the laboratory of research in DNA and biochemical changes in genetic disorders. She is a member of the International Jury L’OREAL-UNESCO Awards « For Women in Science » 2008 - 2015. She supervised around 70 Ph. D. &and master theses. She has more than 100 publications. Peer Reviewer for Scientific Journals.

Abstract:

Autism Spectrum Disorders (ASDs) have become more spread wide over the recent years. In the present study we attempt to unveil the association between ASD and mediators of oxidative stress pathway at the molecular level. We used pathway focused PCR array to analyse gene expression pattern of 84 oxidative stress transcripts in peripheral blood mononuclear cell (PBMC) pools isolated from a total 28 patients with mild/ moderate or severe autism and 16 non-autistic healthy subjects (each sample is a pool from 4 autistic patients or 4 controls). All the participants were diagnosed using; Fourth Edition, Text Revision (DSM-IV-TR), Childhood Autism Rating Scale (CARS) and Autism Diagnosis Intervention- Revised (ADI-R) were done. Only 8 genes showed differential regulation over 1.5 fold change accompanied by statistical significance (p < 0.05) when compared the autistic group to the non-autistic one. The transcriptional profile revealed down regulation of 7 transcripts : Ferritin heavy polypeptide1, Glutamate-cysteine ligase modifier subunit, Neutrophil cytosolic factor2, Prostaglandin-endoperoxide synthase 2, Prion Protein, Superoxide dismutase2 mitochondrial, and Thioredoxin; and up regulation of one gene Glutathione peroxidase 7 in the PBMCs of autistic patients (either mild or severe) compared to controls (p < 0.05 for all). These results suggested that ASD is accompanied by dysregulation of the molecular signals involved in oxidative stress pathway. The current data form the bases for focused studies using single gene expression or custom arrays on a larger number of cases to get the most statistically regulated factors. Acknowledgements for the STDF project for financial support.

Biography:

Dr. Suzanne Tinsley received her PT degree from Texas Woman’s University and earned her PhD in Neuropharmacology from Louisiana State University Health Sciences Center. Dr. Tinsley received her Board Certification in Neurologic Physical Therapy in 2010. She has been on faculty at LSU-Health since 1988 and currently holds the position of Associate Professor. She has published a Pharmacology Text book for physical therapy education. She has an active clinical research program in the area of neurological rehabilitation. Dr. Tinsley has presented her clinical and basic science research in state, national and international scientific forums.

Abstract:

Individuals that suffer from neurological deficits often experience foot drop and knee instability during gait, related to a lack of active control of lower extremity muscles. These impairments combined significantly hinder gait activity and may place the individual at an increased risk for falls. In order to compensate, individuals will often develop compensatory movements that often produce a greater energy cost. Common solutions for foot clearance and knee instability are the use of an ankle-foot orthosis (AFO) and/or functional electrical stimulation (FES) on lower extremity musculature. Advancements in technology have produced FES systems for the lower extremity that can produce a form functional gait cycle. This single-subject repeated measure study design was used to evaluate the short and long term effects of the BioNess L-300® system on joint angles (ankle, knee and hip) in all phases of the gait cycle. The participant (stroke diagnosis) utilized the BioNesss L-300® for gait training activities two times a week for approximately one hour each session over a two year period. Gait parameters using a motion analysis system and outcome measures were recorded at baseline, twelve months and twenty-four months. Results displayed both short term and longitudinal functional improvements in joint angles during all phases of the gait cycle, as well as improvements in all outcome measures. The findings indicated that utilizing the BioNesss L-300® system for gait activities on a limited weekly basis may provide both short term and longitudinal functional improvement in gait activity in individuals with neurological impairments.

Biography:

Cristina Pellegrino Baena (CPB) has completed her PhD in 2013 from PUCPR-Brazil and Erasmus MC- The Netherlands and postdoctoral studies from University of São Paulo- Brazil. She is an Associate Professor in Medicine at PUCPR-Brazil. Raíssa D’Amico (RA) is an outstanding 5th year medicine student. This study is the first cientific project performed by RA and supervised by CPB. CPB has published dozens of papers in high impact journals mostly focusing on epidemiologic aspects of cardiovascular diseases prevention.

Abstract:

Some studies designed to analyze acetylsalicylic acid (ASA) and cardiovascular outcomes reported a protective effect of ASA on chronic migraine. However evidence isn't clear about ASA as a prophylactic agent to migraine. We sought to summarize and analyze evidence on ASA and chronic migraine. Searches in different databases (Medline, Embase, Cochrane, CINAHL, Web of Science, Scopus, Scielo) were conducted for interventions comparing ASA to control in adult populations. Two reviewers selected the articles that met the selection criteria. Disagreements were solved by consensus. Data were extracted about study, population, intervention (dosage, follow up and combined treatment), outcomes (frequency, severity and duration) and quality was evaluated with the Cochrane’s tool. Reported associations were distributed in Harvest Plots, according to outcome, quality and direction of reported associations. We found 458 studies and seven met the selection criteria. A total of 28,326 participants, with ages from 18 to 64 years (96% men). Quality scores ranged from 12 to 16 of 18. Dosages were heterogeneous (100 mg every other day to 650 mg daily). Follow-up from 2 to 72 months. Lack of standardization in units of outcomes and dosage hampered a formal meta-analysis. Regarding frequency, most of the high quality studies (6/7) reported ASA reducing frequency of migraine episodes. Regarding severity and duration most studies (4/5 and 3/4) did not find significant association. Available evidence shows ASA significantly reducing frequency of migraine episodes but not severity or intensity. Future studies designed to analyze ASA and migraine should focus on women, dose response relationship and potential mechanisms.

Biography:

Dr. Morgan earned a BS in Physical Therapy and her academic doctorate in Health Studies in 2006. She has 22 years of rehabilitation experience and has been a faculty member at LSU Health in Shreveport since 1997. She has presented research nationally and internationally on cultural competence, wellness, and neurorehabilitation. She was honored by Maybelline as outstanding female educator and featured in People December 2006 issue. Dr. Morgan was also the 2014 recipient of the Allen A Copping Teaching Award, a finalist for the 2011 International Award for Research and recipient of the APTA Minority Faculty National Scholarship in 2003.

Abstract:

Individuals that suffer from neurological deficits often experience foot drop and knee instability during gait, related to a lack of active control of lower extremity muscles. These impairments combined significantly hinder gait activity and may place the individual at an increased risk for falls. In order to compensate, individuals will often develop compensatory movements that often produce a greater energy cost. Common solutions for foot clearance and knee instability are the use of an ankle-foot orthosis (AFO) and/orfunctional electrical stimulation (FES) onlower extremity musculature. Advancements in technology have produced FES systems for the lower extremity that can produce a form functional gait cycle. This single-subject repeated measure study design was used toevaluate the short and long term effects of the BioNess L-300® system on joint angles (ankle, knee and hip) in all phases of the gait cycle. The participant (stroke diagnosis) utilized the BioNesss L-300® for gait training activities two times a week for approximately one hour each session over a two year period. Gait parameters using a motion analysis system and outcome measures were recorded at baseline, twelve months and twenty-four months. Results displayed both short term and longitudinal functional improvementsin joint angles during all phases of the gait cycle, as well as improvements in all outcome measures. The findings indicated that utilizing the BioNesss L-300® system for gait activities on a limited weekly basis may provide both short term and longitudinal functional improvement in gait activity in individuals with neurological impairments.

Biography:

Dr. Morgan earned a BS in Physical Therapy and her academic doctorate in Health Studies in 2006. She has 22 years of rehabilitation experience and has been a faculty member at LSU Health in Shreveport since 1997.  She has presented research nationally and internationally on cultural competence, wellness, and neurorehabilitation. She was honored by Maybelline as outstanding female educator and featured in People December 2006 issue.  Dr. Morgan was also the 2014 recipient of the Allen A Copping Teaching Award, a finalist for the 2011 International Award for Research and recipient of the APTA Minority Faculty National Scholarship in 2003.

Abstract:

Individuals that suffer from neurological deficits often experience foot drop and knee instability during gait, related to a lack of active control of lower extremity muscles. These impairments combined significantly hinder gait activity and may place the individual at an increased risk for falls. In order to compensate, individuals will often develop compensatory movements that often produce a greater energy cost. Common solutions for foot clearance and knee instability are the use of an ankle-foot orthosis (AFO) and/or functional electrical stimulation (FES) on lower extremity musculature. Advancements in technology have produced FES systems for the lower extremity that can produce a form functional gait cycle. This single-subject repeated measure study design was used to evaluate the short and long term effects of the BioNess L-300® system on joint angles (ankle, knee and hip) in all phases of the gait cycle. The participant (stroke diagnosis) utilized the BioNesss L-300® for gait training activities two times a week for approximately one hour each session over a two year period. Gait parameters using a motion analysis system and outcome measures were recorded at baseline, twelve months and twenty-four months. Results displayed both short term and longitudinal functional improvements in joint angles during all phases of the gait cycle, as well as improvements in all outcome measures. The findings indicated that utilizing the BioNesss L-300® system for gait activities on a limited weekly basis may provide both short term and longitudinal functional improvement in gait activity in individuals with neurological impairments.

Biography:

Dr. Suzanne Tinsley received her PT degree from Texas Woman’s University and earned her PhD in Neuropharmacology from Louisiana State University Health Sciences Center. Dr. Tinsley received her Board Certification in Neurologic Physical Therapy in 2010. She has been on faculty at LSU-Health since 1988 and currently holds the position of Associate Professor. She has published a Pharmacology Text book for physical therapy education. She has an active clinical research program in the area of neurological rehabilitation. Dr. Tinsley has presented her clinical and basic science research in state, national and international scientific forums.

Abstract:

Individuals that suffer from neurological deficits often experience foot drop and knee instability during gait, related to a lack of active control of lower extremity muscles. These impairments combined significantly hinder gait activity and may place the individual at an increased risk for falls. In order to compensate, individuals will often develop compensatory movements that often produce a greater energy cost. Common solutions for foot clearance and knee instability are the use of an ankle-foot orthosis (AFO) and/or functional electrical stimulation (FES) on lower extremity musculature. Advancements in technology have produced FES systems for the lower extremity that can produce a form functional gait cycle. This single-subject repeated measure study design was used to evaluate the short and long term effects of the BioNess L-300® system on joint angles (ankle, knee and hip) in all phases of the gait cycle. The participant (stroke diagnosis) utilized the BioNesss L-300® for gait training activities two times a week for approximately one hour each session over a two year period. Gait parameters using a motion analysis system and outcome measures were recorded at baseline, twelve months and twenty-four months. Results displayed both short term and longitudinal functional improvements in joint angles during all phases of the gait cycle, as well as improvements in all outcome measures. The findings indicated that utilizing the BioNesss L-300® system for gait activities on a limited weekly basis may provide both short term and longitudinal functional improvement in gait activity in individuals with neurological impairments.

Biography:

Yuan-long Pan completed his BVM from Gansu Agricultural University, PR China. He received his PhD in Animal Nutrition from Virginia Tech, USA and PhD in Human Nutrition from UNC-Greensboro, USA. He conducted research in the area of menopause and cognition at Wake Forest University School of Medicine from 1996 to 2000. In 2000, he joined Nestle Purina Research. He has published more than 18 papers, filed 41 patent applications and obtained 10 patents. Recently, he won the Academy of Science-St. Louis 2016 George Engelmann Interdisciplinary Award for his outstanding achievement in science through collaboration

Abstract:

Aging has adverse effects on all tissues and organs in humans and animals including dogs and cats. Just like in humans, some of the senior dogs and cats eventually develop cognitive impairment and dementia called cognitive dysfunction syndrome (CDS). Since CDS is not a curable disease, our research has been focused on nutritional solutions that promote healthy brain aging in dogs and cats for the past 15 years. We have developed two solutions to enhance cognitive functions in dogs and cats. The first approach is to address the reduced ability of brain cells to utilize glucose as energy by providing medium chain triglycerides (MCTs) and we have confirmed that MCTs do enhance cognition in aging dogs. The second solution is to minimize known risk factors associated with brain aging. Since there are multiple risk factors, we have developed a nutrient blend and demonstrated its cognition-enhancing benefits in middle-aged and aging cats. In summary, our research shows that optimal nutrition can enhance cognitive functions in healthy aging dogs and cats. What we have learned from pets may be able to facilitate the development of nutritional and therapeutic solutions for people.

Biography:

Abstract:

The exact mechanisms underlying neuroinflammation and neuropathology in multiple sclerosis (MS) are still unknown, but susceptibility depends on a combination of genetic and environmental risk factors and their interactions. With little influence on genetic predisposition, the importance of modulating environmental risk factors is becoming an area of great interest. There is mounting evidence implicating both late Epstein-Barr virus (EBV) infection and hypovitaminosis-D as key environmental risk factors in MS. We have previously shown that active white matter lesions in the MS brain show signs of innate immune activation and that latently EBV-infected cells can be found in these areas. We hypothesized that EBV-RNAs (EBERs) may get secreted from EBV-infected cells and promote an inflammatory milieu within the lesion. We then tested whether EBV infection was under the control of vitamin-D and found that hypovitaminosis-D, which is a characteristic feature of MS cohorts, was not able to impact on EBV infection. More recently, we compared EBV-status and innate immune signatures in serum and cerebrospial fluid of untreated relapsing-remitting MS patients and found antibody production against latent EBV antigens mainly in the periphery and innate immune IL-8 responses preferentially in the CNS. Dysregulated EBV infection may be a potential risk factor and contribute to MS disease activity via the stimulation of innate immune responses by EBERs, antigenic mimicry and/or cross-reactivity of cellular immune responses with “self” brain antigens or via the transactivation of endogenous retroviruses. The identification of environmental risk factors in MS may offer novel targets for intervention and prevention.

Biography:

Kang Jun Yoon is the Director of MING St. Peter’s Hospital with over 30 years of experience in the medical field since 1984.

Abstract:

The key to successful micro-vascular decompression of the neurovascular compression syndrome is maintaining the separation between the nerve and the offending vessel. We describe a transposition technique in which was mini band retraction for hemi-facial spasm, focusing on the tied-point for transposition the offending artery in the appropriate direction. We conducted a retrospective review of micro-vascular decompression operations in which the offending vessel was transposed and then retained by a designed mini-band, tied from the petrous dura. This technique was used in 42 consecutive cases for 2 years. Post operatively, complete symptom relief was achieved in 97.6% of the patients without any significant surgical complications. No patient suffered recurrence in the follow-up. For mini-designed band retraction technique to be performed successfully, it is important for a mini-band placed at the suitable site to transpose the offending vessel in the intended direction.

Biography:

Kassem El-Shunnar completed his training in Neurosurgery in UK in 1993 following which he took up his first Consultant Neurosurgeon post in January 1994 in Plymouth, Devon. His interest in stereotactic surgery started during his training days in Edinburgh in the late eighties and continued later on with lesional functional neurosurgery and subsequently with image guided surgery. He is now based in the Middle East where he introduced the latest technology in his daily practice.

Abstract:

Introduction: Advances in nasal endoscopy led to cooperation between neurosurgeons and ENT surgeons in Endoscopic trans-sphenoidal Pituitary surgery. This report discusses the cases treated by our team consisting of one neurosurgeon, one ENT surgeon, two endocrinologists and one neuro-ophthalmologist between March 2007 and December 2015. Methods: Forty-four patients (16 females and 28 males) presented to us between March 2007 and December 2015. Age range was 9-80 years. Most patients presented with visual failure. Pituitary apoplexy was the next most common presentation in our series. Hypopituitarism was present in only nine patients. Results: Most cases were non-functioning adenomas. There were 3 Carniopharyngiomas, 2 Rathke's Cleft cysts, 2 prolactinomas, 2 GH secreting tumors and one arachnoid cyst. Two cases had CSF leak requiring repair and 10 cases had transient Diabetes Insipidus. Vision improved in 90% of cases. There was no permanent added impairment to pituitary function. There was no mortality and 2 patients suffered postoperative complications. Conclusions: Endoscopic navigation guided trans-sphenoidal surgery is a safe and reliable procedure. We recommend working as a team of Neurosurgeon and ENT surgeon. We do not recommend preparing a mucosal flap as a routine for each case.

Biography:

Hui-Chieh Lee completed his MD from the National Defense Medical University in 1978 and Undersea Medical Officer Training in Groton USA, in 1979. He had served as the Chief, Dept. of Diving Medicine, Zuoying Naval General Hospital, Taiwan for 10 years and became the President of Hyperbaric and Undersea Medical Association, R.O.C. from 2008 to 2012. Currently, he is the Executive Director of Asian-Pacific Undersea and Hyperbaric Medical Society. He has published 30 papers in the Chinese and International Journal.

Abstract:

Neurological decompression sickness (DCS) is a rare condition that may lead to serious spinal cord injury and sometimes brain injury. We herein report two cases of neurological DCS treated with a combined methods of steroids, hyperbaric oxygen therapy (HBOT), acupuncture and physical therapy. First diving fisherman was a 53-year-old man who developed mental confusion, weakness and numbness over both upper limbs, paraplegia and difficulty urination after a dive to a maximum depth of 38 meters with a total dive time of 60 minutes. The MRI of brain showed multiple acute infarctions of brain. The second diving fisherman was a 45-year-old man who developed chest and back pain, weakness and numbness over right upper limb and both lower limbs with difficulty urination after a dive to 52 meters for 40 minutes. The MRI of spine showed focally increasing signal intensity change of C4-C5 spinal cord region on T2WI. Both cases received one United States Navy (USN) treatment table 6A and one Modified USN table 5A initially and HBOT for 21 sessions and 16 sessions, respectively. The plasma expander and steroids were given before the HBOT. The physical therapy and acupuncture were also applied for rehabilitation of neural function. After discharge, the first case could stand up but still need the help of wheelchair and the second could walk for some distance. Both cases had improvement of urination and defecation. In conclusion, the early examination of MRI for DCS cases with marked neurological symptoms and signs sometimes may show positive findings of brain or spine MRI and a combined method of steroids, HBOT, acupuncture and physical therapy may be useful in the treatment of neurological DCS.

Biography:

Jiatang Zhang has completed his PhD from Medical school of Chinese Peoples’ Liberation Army. He is the Vice-Director of department of neurology at Chinese Peoples’ Liberation Army General Hospital. He has published more than 10 papers in reputed journals.

Abstract:

Background: Limited studies reported the risk of cerebral infarction associated with the change of climate. Our aim is to investigate the risk factors of cerebral infarction occurred after travelling across different climate zones. Methods: Subjects travelled from northeast, northwest and north of China to Sanya during September 1st 2012 to February 28th 2013 were reviewed. Subjects who developed cerebral infarct (Group I) or did not (Group II) were compared and risk factors were identified. Logistic regression models were used to identify the risk factors of cerebral infarction following climate zone change. Results: Two hundred and ninety one subjects (Group I: 144; Group II: 147) were analyzed. Group I patients have higher prevalence of history of cerebral vascular disease, hypertension, abnormal glucose metabolism, and carotid arterial stenosis, hyperhomocysteinemia. Group I also experienced a bigger change of temperature between the place of departure and Sanya. A lower mean arterial blood pressure travel upon arrival to Sanya and a bigger blood pressure difference before and after travel were observed in Group I. Cox regression analysis showed that male gender (OR=1.522, p=0.025), abnormal glucose metabolism (OR=4.617, p<0.001), cerebral arterial stenosis (OR=3.48, p<0.001), hyperhomocysteinemia (OR=1.417, p=0.040), bigger temperature difference between the place of departure and Sanya (each 10°C) (OR=1.423, p<0.001), low blood pressure before travel (OR=0.979, p=0.025) were independent risk factors of cerebral infarction following travel. Conclusions: Cerebral infarction following travel across different climate zones is a newly recognized etiology of stroke, and may be associated with hemodynamic changes.

Biography:

Abstract:

Hereditary deafness comprises a large percentage of all causes of hearing loss. Despite the large number of genetic polymorphisms recognized to cause hereditary deafness, a considerable number of patients do not show any of those. To address the genetic heterogeneity of hereditary hearing loss in Sudanese population, we carried out bioinformatics based analysis of SNPs identified previously by Next Generation Whole Genome Sequencing of three Sudanese patients diagnosed clinically with non-syndromic hereditary deafness. We performed in-silico prediction of the structural and functional effects of polymorphisms noted in known deafness causing genes using SIFT and PolyPhen v2. We further studied the stability and 3D structure of the mutant proteins using iMutant and CPH model, respectively. We were able to identify a set of novel SNPs in deafness associated genes in each patient. Novel polymorphisms in (TRIOBP, TMC1, EYA4) genes were found to have the highest prediction scores in both SIFT and PolyPhen. Those novel SNPs showed decreased predicted stability as well as change in 3D structure models. We consider these novel polymorphisms as candidates for further large scale studies.

Biography:

Guy H Fontaine has made 15 original contributions at the inception of pacemakers since early 60s. He has serendipitously identified Arrhythmogenic Right Ventricular Dysplasia in the late 70s. He has published more than 900 scientific papers including 201 book chapters. He was the reviewer of 17 journals in Clinical and Basic Science. He served during 5 years as a Member of the Editorial Board of Circulation. He has been invited to give 11 master lectures of 90 minutes each during three weeks in the top universities of China (2014).

Abstract:

Therapeutic hypothermia produced by evaporation of Per Fluoro Carbon in the fossa nasalis in a flow of oxygen reported in a prospective multicentre study has demonstrated a tendency to improve outcome in out of hospital cardiac arrest. When I saw the experiments on pigs at the Weil Institute of Cardiac Care Medicine (WICCM), I was immediately convinced that another approach of cooling could be abrupt decompression of gas. After multiple experiments I demonstrated that it was possible to obtain on the same model a drop of brain temperature similar to the work previously reported at the WICCM. However, the simultaneous work on infrared images on severed pig heads suggested that it was possible to cool the brain by the decompression of gas inside the mouth instead of the nose which looks to be an even less invasive and faster method on the field. The second major interest of this new technique seems to be its application in stroke also suggested by animal models. It was during these experiments that my wife watching TV beside me experienced an episode of cardiac arrest that I was able to diagnose immediately. I started Cardio Pulmonary Resuscitation followed by defibrillation performed by an old but still working defibrillator that I kept in the basement of my house when the original study of the method of fulguration was completed. Before arrival of Fire Brigade I used a bottle of compressed gas also available in the basement of my house and delivered the cooling gas at that time in the fossa nasalis. Despite a period of 6 min of no-flow she was able to recover after 5 days of coma with absolutely no neurologic deficit. This fortuitous resuscitation using for the first time brain cooling by decompressed gas will be used for the first pilot study supported by the Schiller Company (Switzerland). It will start soon in the city of Lugano which is already famous for its highest success rate of resuscitation (50%).

Biography:

Dr. Tamiz is a Program Director at the National Institute of Neurological Disorders and Stroke (NINDS), Office of Translational Research (OTR) who oversees NIH Blueprint Neurotherapeutics network (BPN) and Innovation Grants to Nurture Initial Translational Efforts (IGNITE).  

Abstract:

Background: The management of patients with Alzheimer’s disease (AD) is associated with burden and mental health consequences. Main family caregivers are exposed to emotional and physical stress. The burden becomes heavier as the disease progresses, and some caregivers begin to use natural herbal products to improve their mood, anxiety, sleeplessness and vitamins or tonics to improve overall, although in other cases the use of psychotropic drug (i.e., antianxiety, antidepressant, and sedative/hypnotic agents) is required. Objectives: To examine the correlates of psychotropic drug, natural herbal products and vitamins use among family caregivers of AD patients. Other aims were to determine anxiety, and depression. Methods: The study was conducted on a sample group of 175 main family caregivers of AD patients in Galicia (Spain). Caregivers were asked to provide sociodemographic information (Table 1) and information about use of natural herbal products, vitamins and psychotropic drugs. Depressive symptoms were measured using the Beck Depression Inventory-II and anxiety symptoms were measured using the STAI-Anxiety Questionnaire (Table 2). Results: The analysis of the results shows that the average caregiver of an AD patient is a woman, approximately 56 years old. The majority of caregivers are sons/daughters (65%) with a primary education (37.1%). The prevalence of psychotropic drug use among caregivers (39%) is higher than previously reported prevalence rates in the general population. Of caregivers with depressive symptoms, 52% used psychotropic drug. Of caregivers with anxiety symptoms 44.6% used psychotropic drug. 31.4% of caregivers used natural herbal products and 14.3% of caregivers used vitamins or tonics to improve overall. The use of natural herbal products in women caregivers (36%) was higher than men caregivers (17%). Conclusion: This study found that 48% of caregivers with depressive symptoms and 55.4% of caregivers with depressive symptoms were not taking psychotropic drug, even with high levels. Results suggest that routine screening for depression and anxiety in caregivers may identify unmet needs for antidepressant therapy and may provide help caregivers.

The mission of the Office of Translational Research (OTR) within the National Institute of Neurological Disorders and Stroke (NINDS) is to accelerate the preclinical discovery and development of new therapeutic interventions for neurological disorders. The NINDS is part of the National Institutes of Health (NIH), the leading supporter of biomedical research in the world. The OTR provides funding (approximately $100 million annually) and resources through grants, cooperative agreements, and contracts to industry and university researchers to advance early-stage neurological technologies, devices, and therapeutic programs to industry adoption (i.e., investor funding and corporate partnerships). The OTR comprises five programs that support the design, implementation, and management of research activities to critical translational challenges in neurology.

Biography:

Abstract:

Migraine-like cerebral transient ischemic attacks (MIAs) and ocular ischemic manifestations were the main presenting features in 10 JAK2 V617F -positive patients studied, with essential thrombocythemia (ET) in 6 and polycythemia vera (PV) in 4. Symptoms varied and included cerebral ischemic attacks, mental concentration disturbances followed by throbbing headaches, nausea, vomiting, syncope or even seizures. MIAs were frequently preceded or followed by ocular ischemic events of blurred vision, scotomas, transient flashing of the eyes, and sudden transient partial blindness preceded or followed erythromelalgia in the toes or fingers. The time lapse between the first symptoms of aspirin-responsive MIAs and the diagnosis of ET in 5 patients ranged from 4 to 12 years. At the time of erythromelalgia and MIAs, shortened platelet survival, an increase in the levels of the platelet activation markers β-thromboglobulin and platelet factor 4 and also in urinary thromboxane B2 were clearly indicative of the spontaneous in vivo platelet activation of constitutively JAK2 V617F -activated thrombocythemic platelets. Aspirin relieves the peripheral, cerebral and ocular ischemic disturbances by irreversible inhibition of platelet cyclooxygenase (COX-1) activity and aggregation ex vivo. Vitamin K antagonist, dipyridamole, ticlopidine, sulfinpyrazone and sodium salicylate have no effect on platelet COX-1 activity and are ineffective in the treatment of thrombocythemiaspecific manifestations of erythromelalgia and atypical MIAs. If not treated with aspirin, ET and PV patients are at a high risk of major arterial thrombosis including stroke, myocardial infarction and digital gangrene

Biography:

Dr Oliver Tolson completed his medical degree at Newcastle University Medical School, following completion of his Masters in Research in 2014. He was awarded a Wolfson Intercalated Award in 2013 to fund this research into fatigue and autonomic dysfunction in multiple sclerosis. Prof Julia Newton completed her medical degree in 1990. During her academic career she has gone on to publish several prominent papers in the field of fatigue and autonomic dysfunction, in diseases such as primary biliary cirrhosis and chronic fatigue syndrome. She currently is the Dean of Clinical Medicine and Professor of Ageing and Medicine at Newcastle University, UK. Project design and analysis was conducted under her supervision, utilising her experience and expertise in the area.

Abstract:

Background: Fatigue is a common debilitating symptom of multiple sclerosis (MS) but its pathophysiology remains poorly understood. Recent studies in a variety of diseases have shown dysfunction of the cardiovascular autonomic nervous system correlates with fatigue severity. Objectives: To investigate the prevalence of fatigue and orthostatic intolerance in a representative MS cohort. To objectively assess fatigued secondary-progressive patients for cardiovascular autonomic dysfunction. Methods: Fatigue severity and orthostatic intolerance were measured using validated questionnaires in 144 patients (85.2% response). Subsequently, 11 fatigued secondary-progressive MS patients underwent objective assessment of resting heart rate variability (HRV) and blood pressure variability (BPV). Results: Fatigue was identified in 74.8% of MS patients, with fatigue severity significantly higher in secondary-progressive patients. Moderate orthostatic intolerance was identified in 54.3% of patients and correlated significantly with fatigue (r=0.49, p<0.0001). Objective assessment revealed significant reductions in low-frequency HRV and BPV in the fatigued secondary-progressive group versus controls. A substantial reduction was seen in low-frequency systolic BPV (33.6% versus 48.9%, p=0.03), an established marker of sympathetic vasomotor function. Furthermore reductions in this parameter correlated significantly with orthostatic symptoms (r=−0.87, p=0.0007) and fatigue severity (r=−0.66, p=0.03). Conclusions: Fatigue severity correlates significantly with increasing orthostatic intolerance. Additionally, fatigued secondary-progressive patients have objective evidence of sympathetic vasomotor dysfunction.

Biography:

Hanan Azouz has completed her Doctorate Degree of Pediatrics in 1994 from Alexandria University and PhD of health of children with special needs from Ain Shams University, Egypt. She is professor and head of Neuropediatrics and Behavioral Pediatrics unit in Faculty of Medicine, Alexandria University. She supervised over 30 researches and shared in adaptation of guidelines for ADHD and ASD in Alexandria. She is a member in ICNA and she was the secretary of congress of Egyptian Society of child Neuro-Psychiatry and Pan-Arab child neurology association. She has published more than 10 papers in reputed journals.

Abstract:

Autistic spectrum disorder (ASD) is a neurodevelopmental disorder characterized by a behavioral phenotype that includes qualitative impairment in the areas of language development or communication skills, social interactions and reciprocity, and restricted repetitive behavior. Normal function of the auditory sensory organs and the central auditory pathways is a prerequisite for the normal development of language. In autism, deficits in language, particularly delays in language acquisition, are the principal early manifestation of the disorder. The range of language abilities varies from total muteness to the use of an apparent grammatically complex language. The auditory profile at different levels of the auditory system in children with ASD and the role of (Central) auditory processing (CAP) disorder as an essential pathology of the autistic disorder or as an associated co-morbidity was studied on thirty children, as well as the correlation between CAP findings and the language delay in these cases. 40% of the children with ASD were hyper-responsive to auditory stimuli according to the Sensory checklist for auditory skills. ABR showed interpeak latencies (IPLs) I–V and III–V of both ears were significantly prolonged in the ASD group in addition to absolute latency of wave I of the left ear and absolute latency of wave V in right ear were significantly prolonged in the ASD group. The results concluded that (central) auditory processing disorder is an essential pathology of the autistic disorder. Autistic children possess a dysfunctioning or an immature central auditory nervous system at both the brainstem and cortical levels.

Biography:

Geoffrey Burnstock completed his PhD at King's College and University College London. He was head of the Department of Zoology, Melbourne University (1964-1975) before moving to London to head the Department of Anatomy and Developmental Biology, UCL until 1997. He is currently the President of the Autonomic Neuroscience Centre, University College Medical School, UK. He is a Fellow of the Australian Academy of Sciences (1971), Royal Society (1986) and Academy of Medical Sciences (1998). He was awarded the Royal Society Gold Medal (2000) and has over 1520 publications and an H-index of 135.

Abstract:

The concept of purinergic neurotransmission (i.e. neurally released ATP acting as an extracellular signaling molecule) was proposed in 1972. Later it was recognized as a co-transmitter in most, if not all, nerves in the peripheral and central nervous systems, acting on post- and also pre-junctional membranes, at autonomic neuro-effector junctions and ganglionic and central synapses. ATP and its breakdown product adenosine also act as trophic factors during development and regeneration. Brief background information is given about ATP storage, release and ecto-enzymatic breakdown. Purines and pyrimidines have key roles in neurotransmission and neuro-modulation, with their effects being mediated by P1 (adenosine), P2X ion channel and P2Y G protein-coupled receptors. There is coverage of neuron-glia interactions and of purinergic neuro-effector transmission to non-muscular cells. Purinergic mechanisms and specific receptor subtypes have been shown to be involved in pathological conditions, including brain trauma and ischemia, epilepsy, visceral and neuropathic pain, neurodegenerative diseases associated with neuro-immune and neuro-inflammatory reactions, as well as neuropsychiatric diseases, including depression, anxiety and schizophrenia. Specific purinergic receptor subtypes, notably A2A, P2X4 and P2X7 are being explored as therapeutic targets for the treatment of these conditions.

Biography:

Shao-Jun Tang completed his PhD from the University of Toronto in Canada in 1998 and Post-doctoral studies from the HHMI/California Institute of Technology in USA in 2001. He is currently the William Willis Jr. MD PhD Distinguished Professor in Neuroscience and the Director of Neuroscience Graduate Program in the University of Texas Medical Branch

Abstract:

Neuropathic pain is a common neurological disorder in HIV-1/AIDS patients. Current therapies for HIV-associated neuropathic pain are largelyineffective. Multiple etiological factors may contribute to the pathogenesis of this pain syndrome, including HIV-1 infection and antiretroviral medicine. Analysis of the pain neural pathway in postmortem tissues of HIV-infected patients leads to identifying specific neuropathologies that may causally link to pain development in the patients.We are interested in understanding the pathogenic mechanism for the ultimate development of rationale-based therapeutic approaches. Our work has been focused on identifying the HIV-1 pathogenic factor and elucidating the molecular and cellular processes through which the factor causes neuropathic pain. We have undertaken an interdisciplinary approach in this research, including analyzing postmortem nervous tissues from HIV-1/AIDS patients, generating clinically relevant rodent models, and determining the molecular, cellular, behavioral and electrophysiological abnormalities in the model. Our results indicate that HIV-1 gp120 is a relevant viral factor for the HIV neuropathic pain. We also identify that that Wnt signaling in the pain neural circuit plays a key role in mediating the activity of gp120 to cause major neuropathologies of HIV-associated pain such as neuro-inflammation, astroglial reaction and neuropathy.Our studies may provide novel insights into the molecular, cellular and circuitry mechanisms of HIV-associated neuropathic pain.

Biography:

Safa Shehab has completed his PhD in Sheffield University. He served in several universities in UK including UMIST, Sheffield, Glasgow and Aberdeen before he joined UAE University. He investigates the neuronal circuitry in the dorsal horn of the spinal cord and the neuronal pathways that are likely to be critical in the production and maintenance of the neuropathic pain after peripheral nerve injury. He is also investigating the mechanism of Deep Brain Stimulation. He has published 48 papers in reputed journals.

Abstract:

Rats develop hyperalgesia and allodynia in the hind paw following L5 spinal nerve ligation and transection as seen in human neuropathic pain. Since the skin of the hind paw of the rat is mainly innervated by L4 and L5 nerves, it is assumed that uninjured L4 nerve would be involved in the development of neuropathic pain. Anatomically, we showed that the unmyelinated primary afferents of L5 spinal nerve did not only terminate in the corresponding L5 spinal segment and rather extended to two spinal segments rostrally and one segment caudally where they intermingle with primary afferents of L4 nerve. Subsequently, we demonstrated up-regulations of NPY, VIP and NK1r and down-regulations of SP, CGRP and IB4 binding following L5 nerve injury not only in the dorsal horn of L5 spinal segment where the injured L5 enters, but also extended from L3-L6 spinal segments. To investigate the potential role of adjacent uninjured L4 nerve in heat hyperalgesia, Phosphorylated Extracellular Regulated Kinase (pERK) was used as a pain marker in response to heat noxious stimuli applied to both hind paws following unilateral L5 nerve injury. The results showed that the number of pERK-immunoreactive neurons was significantly higher in the ipsilateral side of L4 spinal segment, which receives innervation from uninjured L4 nerve, compared with contralateral control side which receives both uninjured L4 and L5 spinal nerves. The data demonstrate the role of uninjured L4 nerve in the development of heat hyperalgesia following L5 nerve injury. Two hypotheses on the production and maintenance of peripheral neuropathic pain will be discussed.

Biography:

David Moore is a Post-doctoral research fellow at the Department of Pain Medicine, St James Hospital, Dublin and the Institute of Neurotherapeutics, Dublin City University.

Abstract:

Neuropathic pain poses a significant burden on the individual and society, because of a lack of effective pharmacological therapies. Interventional pain therapies may be more effective in a select cohort of patients. Neuropathic pain results from a lesion or disease of the somatosensory system. Traditionally neuropathic pain was attributed to dysfunctional activity and hypersensitivity of the neuron. However a maladaptive immune response is increasingly recognized as contributing to the maintenance of chronic neuropathic pain. Glial cell activation and altered peptide biosynthesis are implicated in the maintenance of persistent neuropathic pain. Human data suggests that NGF, VEGF and BDNF play a role here. This neuroimmune process is maintained by cellular and neuropeptide biosynthetic responses which become pathological. Intra-thecal opioids and steroids are associated with alterations in cell signaling and the levels of inflammatory mediators at the neuroimmune interface in humans in vivo. Markers of glial and immune cell activity, up-regulated in neuropathic pain states, are down-regulated in spinal cord stimulator patients. Pulsed radiofrequency of the dorsal root ganglion in patients with radicular pain alters CSF lymphocyte subsets and peptide concentrations

Biography:

Hui-Chieh Lee completed his MD from the National Defense Medical University in 1978 and Undersea Medical Officer Training in Groton USA, in 1979. He had served as the Chief , Dept. of Diving Medicine, Zuoying Naval General Hospital, Taiwan for 10 years and became the President of Hyperbaric and Undersea Medical Association, R.O.C. from 2008 to 2012. Currently, he is the Executive Director of Asian-Pacific Undersea and Hyperbaric Medical Society. He has published 30 papers in the Chinese and International Journal.

Abstract:

Neurological decompression sickness (DCS) is a rare condition that commonly leads to spinal cord injury. We report the case of a 30-year-old man who developed left-sided weakness and numbness after diving to a maximum depth of 15 m with a total dive time of 205 min (10 repetitive dives). To the best of our knowledge, only six cases diagnosed as Brown-Séquard syndrome caused by DCS have been reported in the literature. Divers should be aware of the risk factors of DCS before diving and clinicians should make the diagnosis of spinal cord DCS based primarily on clinical symptoms, not on magnetic resonance imaging findings.

Biography:

Mirjana Djukic has completed her PhD in 2001 at the Faculty of Pharmacy at the University of Belgrade. She became a full Professor of Toxicology in 2012. Her research interest has focused on free radicals-mediated mechanism pathways of drugs/poisonings. Accordingly, on oxidative stress-related topics she introduced an optional subject in the faculty study program (2008); wrote (author and editor) two books; published/presented cc 190 papers and has been reviewing articles to reputable journals. She spent two years in the Center for Free Radical and Antioxidant Health (Prof. Valerian Kagan lab) at the University Pittsburgh, USA (2002/3, 2010/11).

Abstract:

Paraquat (PQ) neurotoxicity has not thoroughly investigated. Redox metabolism of PQ2+, results in superoxide anion radical (O2•ï€­) formation. Consequent free radical reactions escalate due to stable resonance radical structure (PQ•+). The OS/NS-associated neurotoxic pathways of PQ were investigated in striatum of Wistar rats after single intra-striatal administration of PQ+ and applied pretreatments, including: N-nitro-L-arginine-methyl ester (L-NAME); 2-amino-5-phosphonovaleric acid (APV); glutathione reductase (GR) and naloxone. Reversible Parkinson’s disease symptoms were observed in PQ group. Contrary to PQ, APV+PQ and GR+PQ groups, initially high O2•ï€­ reached the normal values in L-name+PQ and naloxone+PQ groups, on 7thday. Superoxide dismutase (SOD) activity declined in L-name+PQ, naloxone+PQ and APV+PQ groups. Initially low SOD activity reached normal values on 7th day in Pq and GR+PQ groups. Lipid peroxidation was the highest in PQ, L-name+PQ and GR+PQ groups. Glutathione (GSH) depletion was considerable in L-name, APV and naloxone pretreated rats across the time. Increased GSH values were achieved in PQ and GR+PQ group on the 7th day. Glutathione peroxidase (GPx) activity was inhibited by GR (within 24 hours) and naloxone; elevated GPx activity declined with the time in APV+PQ and L-name+PQ; while it was high in PQ group until the 7th day. In conclusion, inhibitors of NO-synthase, N-methyl-D-aspartate (NMDA) and opioid receptors, reduced SOD and GPx activities and depleted GSH. Rise of O2•ï€­ occurred in APV and GR pretreated groups (twice higher than in PQ group), on 7th day, although APV did not influence LPO.

Biography:

Abstract:

Dietary omega-3 fatty acids have been recognized to improve brain cognitive function. Deficiency leads to dysfunctional zinc metabolism associated with learning and memory impairment. The objective of this study is to explore the effect of short-term dietary omega-3 fatty acids on hippocampus gene expression at the molecular level in relation to spatial recognition memory in mice. A total of 24 male BALB/c mice were randomly divided into four groups and fed a standard pellet as a control group (CTL, n=6), standard pellet added with 10% (w/w) fish oil (FO, n=6), 10% (w/w) soybean oil (SO, n=6) and 10% (w/w) butter (BT, n=6). After 3 weeks on the treatment diets, spatial-recognition memory was tested on a Y-maze. The hippocampus gene expression was determined using a real-time PCR. The results showed that 3 weeks of dietary omega-3 fatty acid supplementation improved cognitive performance along with the up-regulation of α-synuclein, calmodulin and transthyretin genes expression. In addition, dietary omega-3 fatty acid deficiency increased the level of ZnT3 gene and subsequently reduced cognitive performance in mice. These results indicate that the increased the ZnT3 levels caused by the deficiency of omega-3 fatty acids produced an abnormal zinc metabolism that in turn impaired the brain cognitive performance in mice.

Biography:

Abstract:

Dietary omega-3 fatty acids have been recognized to improve brain cognitive function. Deficiency leads to dysfunctional zinc metabolism associated with learning and memory impairment. The objective of this study is to explore the effect of short-term dietary omega-3 fatty acids on hippocampus gene expression at the molecular level in relation to spatial recognition memory in mice. A total of 24 male BALB/c mice were randomly divided into four groups and fed a standard pellet as a control group (CTL, n=6), standard pellet added with 10% (w/w) fish oil (FO, n=6), 10% (w/w) soybean oil (SO, n=6) and 10% (w/w) butter (BT, n=6). After 3 weeks on the treatment diets, spatial-recognition memory was tested on a Y-maze. The hippocampus gene expression was determined using a real-time PCR. The results showed that 3 weeks of dietary omega-3 fatty acid supplementation improved cognitive performance along with the up-regulation of α-synuclein, calmodulin and transthyretin genes expression. In addition, dietary omega-3 fatty acid deficiency increased the level of ZnT3 gene and subsequently reduced cognitive performance in mice. These results indicate that the increased the ZnT3 levels caused by the deficiency of omega-3 fatty acids produced an abnormal zinc metabolism that in turn impaired the brain cognitive performance in mice.

Biography:

Abstract:

Deafness is the most frequent sensory deficit in humans. The etiology is genetic in about half of the cases worldwide. The most frequent cause of non-syndromic autosomal recessive deafness is an altered connex in 26-protein, a communicating gap junction protein encoded by the gene GJB2. Previous studies included Sudanese and Kenyan patients suggested other causes for hearing impairment other than GJB2. Two Sudanese patients with a prelingual, profound, sensorineural, bilateral, non-syndromic hearing loss were screened for GJB2 using DNA extracted from blood which was followed by PCR and sequencing. The patients had different frame shift mutations that were unreported before

Biography:

Dr. Ramel Carlos has been working as a neurologist in the Island of Guam for the past 13 years. He completed his Neurology residency and Epilepsy and Clinical Neurophysiology fellowship training at Wake Forest University, Winston Salem, North Carolina, USA. Noel Bien Carlos is currently a Neuroscience student at the University of Southern California in Los Angeles, California. He is actively involved in clinical and laboratory research.

Abstract:

The risk of cardiovascular and cerebrovascular diseases, as well as neurodegenerative diseases such as dementia and Parkinson disease (PD) increases with aging. Numerous researches have shown that these vascular diseases may be influential in increasing the risk of developing neurodegenerative diseases. This study aims to determine the occurrences of vascular diseases in patients with dementia and PD in the Island of Guam. This is a retrospective review of medical records of patients in the only Neurology Clinic in Guam with the diagnosis with dementia and PD from August 2006 to December 2014. There were 348 patients with dementia and 206 patients with PD. The mean age of diagnosis for patients with dementia is higher for both genders than PD patients. There were more females (60%) diagnosed with dementia while more males (61%) have PD. Hypertension, diabetes mellitus, hyper-lipidemia, heart disease and stroke were identified in 76%, 49%, 60%, 30%, and 35% of patients with Dementia, respectively. In addition, Hypertension, Diabetes Mellitus, Hyperlipidemia, Heart Disease and Stroke were identified in 80%, 50%, 58%, 21%, and 29% of patients with PD, respectively. There is an increased occurrence of various vascular diseases in patients with dementia and PD in Guam. It is recommended to optimally control these vascular diseases early on at the diagnosis to potentially prevent progression of neurodegenerative diseases. It is also recommended to implement an awareness program in Guam to educate the public in prevention and treatment of vascular diseases, which are highly prevalent in neurodegenerative diseases.

Biography:

Suzanne L Tinsley received her PT degree from Texas Woman’s University and earned her PhD in Neuro-pharmacology from Louisiana State University Health Sciences Center. She received her Board Certification in Neurologic Physical Therapy from ABPTS. She has been on faculty at LSU-Health since 1988 and currently holds the position of Associate Professor. She has published a Pharmacology Text book for physical therapy education. She has an active clinical research program in the area of neurological rehabilitation. She has presented her clinical and basic science research in state, national and international scientific forums.

Abstract:

Individuals that suffer from neurological deficits often experience foot drop and knee instability during gait, related to a lack of active control of lower extremity muscles. These impairments combined, significantly hinder gait activity and may place the individual at an increased risk for falls. In order to compensate, individuals will often develop compensatory movements that often produce a greater energy cost. Common solutions for foot clearance and knee instability are the use of an ankle-foot orthosis (AFO) and/or functional electrical stimulation (FES) on lower extremity musculature. Advancements in technology have produced FES systems for the lower extremity that can produce a functional gait cycle. This descriptive study evaluates the BioNesss L-300 Plus® system effectiveness for individuals with neurological gait deficits. Two participants with neurological impairments, using a repeated measures within-subject design, took part in one session of motion analysis data collection measuring joint angles at the hip, knee and ankle. The resulting joint angles were compared during 4 phases of the gait cycle in three different environments: without FES, with BioNesss L-300® (calf only), and with BioNesss L-300 Plus® (calf and thigh). Study results indicate improved joint angles and more activity in hip musculature with the using the BioNesss L-300 Plus® system for both participants as well as immediate improvements in gait speed. These findings indicate a possible improved and more efficient gait pattern, as well as more appropriate joint angles in all phases of the gait cycle by utilizing both the BioNesss L-300 Plus® system

Biography:

Dr. Gratwicke qualified in medicine from the University of Oxford, and undertook post-graduate training in neurology at the National Hospital for Neurology and Neurosurgery in Queen Square, London. He is a practicing neurologist both at NHNN, Queen Square and St. George’s Hospital in south London, with specialist interests in movement disorders, dementia and neurodegenerative diseases. He is concurrently completing a PhD at UCL’s Institute of Neurology where he works within the Unit of Functional Neurosurgery, delivering both a specialist academic and clinical DBS service to patients. He has published a number of highly cited papers in reputed journals discussing cognitive network dysfunction in dementias and the use of cognitive neuromodulation as a therapy to counter this.

Abstract:

Dementia remains one of the major challenges facing western society with an estimated 80 million people due to be affected by 2040. Despite this only a handful of modestly effective symptomatic therapies exist. Recent trials of pharmacologic agents aimed at reducing aggregation of pathogenic proteins have proved ineffective, likely because of the heterogeneity of the genetic and molecular pathology underlying dementia syndromes, and novel approaches are therefore needed. Brain stimulation therapies can avoid these difficulties by modulating the disease process downstream at the neural network level, aiming to restore cognitive processing patterns and thereby relieve symptoms. In this presentation I will discuss how improved understanding of cognitive brain networks can be harnessed for development of novel brain stimulation therapies for dementia, with a particular focus on the use of deep brain stimulation. I will cover both basic scientific and clinical aspects of this approach, and discuss the results of two clinical trials recently completed in our unit. I will also look to the future and discuss how cognitive neuromodulation can be advanced further through improved understanding of brain functioning, from both empirically driven and computationally driven approaches.

Biography:

Sybille Krauß studied biotechnology at the Technische Fachhochschule Berlin until 2002. As graduate student she worked at the Max Planck Institute for Molecular Genetics and received her PhD in 2005. After this, she conducted research as postdoc at the Charité in Berlin in the group of Prof. Susann Schweiger. Since 2010 Sybille Krauß is groupleader at DZNE in Bonn.

Abstract:

Polyglutamine diseases are monogenic diseases that are caused by elongation of CAG repeat motifs translating into elongated polyglutamine (polyQ) stretches on the protein level. Aggregation polyQ proteins in the central nervous system of patients is a hallmark of polyQ diseases. Based on the neurotoxic function of these proteins produced from expanded CAG repeats, a reduction of these proteins will be beneficial in the disease context. In line, reduction of polyglutamine protein in disease models for polyglutamine diseases improved the disease phenotype. But how is the protein synthesis rate from expanded CAG repeat mRNAs regulated? One mechanism that we have recently identified to play a role in regulating the translation of huntingtin (HTT) mRNA with expanded CAG repeats involves the MID1-PP2A complex. Mutant HTT mRNA binds to a protein complex containing the MID1 protein, the catalytic subunit of protein phosphatase 2A (PP2Ac), and 40S ribosomal S6 kinase (S6K) in a CAG repeat length-dependent manner. Strikingly, binding of the MID1 protein complex to mutant HTT mRNA results in an increased translation and subsequently aggregation of mutant HTT. Interestingly, this sequestration of MID1 to expanded CAG repeats does not seem to be limited to mutant HTT mRNA, but is also seen on other mRNAs with expanded CAG repeats such as mutant ATXN3. This makes the MID1-RNA-protein complex a very interesting target to prevent formation of pathological accumulations of mutant polyQ protein in polyQ disorders.

Biography:

Dr Oliver Tolson completed his medical degree at Newcastle University Medical School, following completion of his Masters in Research in 2014. He was awarded a Wolfson Intercalated Award in 2013 to fund this research into fatigue and autonomic dysfunction in multiple sclerosis.

Abstract:

Background: Fatigue is a common debilitating symptom of multiple sclerosis (MS) but its pathophysiology remains poorly understood. Recent studies in a variety of diseases have shown dysfunction of the cardiovascular autonomic nervous system correlates with fatigue severity. Objectives: To investigate the prevalence of fatigue and orthostatic intolerance in a representative MS cohort. To objectively assess fatigued secondary-progressive patients for cardiovascular autonomic dysfunction. Methods: Fatigue severity and orthostatic intolerance were measured using validated questionnaires in 144 patients (85.2% response). Subsequently, 11 fatigued secondary-progressive MS patients underwent objective assessment of resting heart rate variability (HRV) and blood pressure variability (BPV). Results: Fatigue was identified in 74.8% of MS patients, with fatigue severity significantly higher in secondary-progressive patients. Moderate orthostatic intolerance was identified in 54.3% of patients and correlated significantly with fatigue (r=0.49, p<0.0001). Objective assessment revealed significant reductions in low-frequency HRV and BPV in the fatigued secondary-progressive group versus controls. A substantial reduction was seen in low-frequency systolic BPV (33.6% versus 48.9%, p=0.03), an established marker of sympathetic vasomotor function. Furthermore reductions in this parameter correlated significantly with orthostatic symptoms (r=−0.87, p=0.0007) and fatigue severity (r=−0.66, p=0.03). Conclusions: Fatigue severity correlates significantly with increasing orthostatic intolerance. Additionally, fatigued secondary-progressive patients have objective evidence of sympathetic vasomotor dysfunction.

Biography:

Bulent Unay has completed his PhD from Medical School and currently working as Child Neurology Professor in Department of Pediatrics. He had the position of Research Fellow in Epilepsy Center, Children’s Hospital; University of Pittsburgh from 2004 to 2005. He is the Director of Department of Child Neurology. He has published more than 65 peer reviewed medical articles and book chapters on many topics including epilepsy, evoked potentials and cerebral palsy.

Abstract:

Occipital intermittent rhythmic delta activity (OIRDA) may be present either in physiological or pathological conditions. Absence seizures present as brief episodes of staring and unresponsiveness and are characterized by an abrupt cessation of activity and impairment of consciousness. Generalized 2.5–4 Hz spike and wave discharges are electrographic pattern of absence epilepsy. OIRDA occurs usually in children. OIRDA was described in patients with epilepsy, particularly with generalized syndromes, such as absence epilepsy. In this report we present a patient with absence epilepsy who have OIRDA findings in their EEG recording and discussed the clinical importance of OIRDA in children. Posterior slow activity on EEG was initially described in children with behavior problems. Throughout the years, the range of clinical interpretation of this pattern by researchers varied to suggesting non-specific, metabolic, epileptic and structural. 7-year old boy who met the diagnostic criteria for absence epilepsy admitted to epilepsy center of university hospital. Absence was defined based on ILAE classification. OIRDA was defined as intermittent monomorphic rhythmic delta activity with maximal amplitude over the occipital regions ranging from 1-4 Hz. He had one record of awaken EEG where OIRDA was reported and sleep EEG was normal. OIRDA ranged from 1-2 Hz to 2-3 Hz in same record. In previous studies, OIRDA was found in 3-4 % of children. OIRDA may not be associated to structural lesions and was described in patients with absence seizures by Cobb in 1945. Recently (2003) Gullapali and Fountain reported a series of 77 patients with OIRDA and found seizures to be more frequent than in the control group. Some authors consider OIRDA as a good prognosis factor in patients with absences.

Biography:

Hanan Galal Azouz has completed her Doctorate Degree of Pediatrics in 1994 from Alexandria University and PhD of health of children with special needs from Ain Shams University, Egypt. She is Professor and Head of Neuro-pediatrics and Behavioral Pediatrics unit in Faculty of Medicine, Alexandria University. She supervised over 30 researches and shared in adaptation of guidelines for ADHD and ASD in Alexandria. She is a member in ICNA and was the secretary of congress of Egyptian Society of Child Neuro-Psychiatry and Pan-Arab Child Neurology Association. She has published more than 10 papers in reputed journals

Abstract:

Autistic spectrum disorder (ASD) is a neuro-developmental disorder characterized by a behavioral phenotype that includes qualitative impairment in the areas of language development or communication skills, social interactions and reciprocity and restricted repetitive behavior. Normal function of the auditory sensory organs and the central auditory pathways is a prerequisite for the normal development of language. In autism, deficits in language, particularly delays in language acquisition, are the principal early manifestation of the disorder. The range of language abilities varies from total muteness to the use of an apparent grammatically complex language. The auditory profile at different levels of the auditory system in children with ASD and the role of (Central) auditory processing (CAP) disorder as an essential pathology of the autistic disorder or as an associated co-morbidity was studied on thirty children, as well as the correlation between CAP findings and the language delay in these cases. 40% of the children with ASD were hyper-responsive to auditory stimuli according to the Sensory checklist for auditory skills. ABR showed inter-peak latencies (IPLs) I–V and III–V of both ears were significantly prolonged in the ASD group in addition to absolute latency of wave I of the left ear and absolute latency of wave V in right ear were significantly prolonged in the ASD group. The results concluded that (central) auditory processing disorder is an essential pathology of the autistic disorder. Autistic children possess a dysfunctioning or an immature central auditory nervous system at both the brainstem and cortical levels.

Biography:

Natalia Vérez Cotelo has completed her PharmD from Santiago de Compostela University and Post-doctoral studies from Universidad Nacional de Educación a Distancia (UNED) School of Phsycology. She is member of Berbés Group, a Pharmaceutical Research and Education organization. She has published more than 25 papers in reputed journals and has been serving as Pharmacist in National Health Service in Spain.

Abstract:

In Spain, as in other Mediterranean countries, family caregivers play an essential role in caring for patients with Alzheimer’s disease (AD). Given the high demands on caregivers of AD patients, they may experience physical, psychological or social consequences as a result of caregiving. Several factors are associated with the onset of caregiver burden, including the social support available, AD patient’s health, and the place where they live. A cross-sectional study with 175 family informal caregivers was conducted at a community pharmacy and in family caregivers associations in Galicia (Spain). Demographic variables were collected, and the following questionnaires were administered: the Beck Depression Inventory-II, STAI-Anxiety Questionnaire, Zarit Burden Scale, family APGAR scale, and the Duke-UNC questionnaire. The typical caregiver profile consists of a 56-year old women with a primary education who belongs to a functional family. Nearly a half (48%) of caregivers had a high perception of burden, with anxiety in 37% of caregivers and symptoms of depression in 25%. Family caregivers usually went to the same pharmacy (93%), were treated with psychotropic drugs (39%) and interacted with the pharmacist (90%). The caregivers from cities of The Atlantic Ocean zone presented a major level of overload and anxiety that those of the interior of Galicia. The caregiver members of family caregivers associations showed major overload and anxious symptoms that those who aren´t members of any association. The cultural standard, a good familiar function and the social received support act as "protective" factors. This study confirmed that pharmacists can help caregivers finding signs of psychopathology in order to improve their psychological health.

Biography:

Prof. Villa graduated in Biological Sciences (D.Sc.) and in Medicine and Surgery (M.D.); he is Associate Professor of Pharmacology at University of Pavia. His research activities on the cerebral energy metabolism evaluated by the Functional Proteomics and Metabolomics are about the Physiopathology and Pharmacology of the Central Nervous System in experimental conditions of hypoxia, ischemia, hyperammoniemia, hypoglycemia; molecular mechanisms of aging and drugs' interference; the study of Parkinson’s disease and drugs' actions in Dementia, clinical studies on Molecular Medicine and Human Genetics on patients affected by Dementias and Ischaemia. He published 349 total papers (IF about 350) and has been officially invited to 214 Congress since 1993.

Abstract:

Acute ischaemic stroke (AIS) is a leading cause of death and disability worldwide. Its incidence and prevalence increase considerably with age and numbers of patients will grow in the future. AIS is caused by the abrupt occlusion of an intracranial vessel resulting in reduced blood flow to the brain region supplied. The ischemic core (which is irreversibly lesioned) is surrounded by the penumbra region with less severe flow reduction, lower functional impairment and potential recovery; so, the fundamental treatment of AIS relies on prompt recanalisation and reperfusion of the threatened ischemic penumbra, that however is potentially salvageable. With this aim, intravenous thrombolysis with recombinant tissue plasminogen activator (rtPA) remains the current strategy. However, thrombolysis is underused, owing to various exclusion criteria that limit the number of treated patients. Other thrombolytics are under investigation. Endovascular therapy with mechanical recanalisation devices is increasingly applied; moreover, hypertension and hyperglycemia are acute complications to be treated in AIS. Our study analyzes the current status, the problems, the perspectives of the pharmacological therapy for AIS.

Biography:

Abstract:

Background: Impairment in cognitive functioning and motor activity are commonly encountered in patients affected by multiple sclerosis (MS). Objective: To investigate the effect of enhanced environment on cuprizone mouse model of demyelination. Methods: C57BL/6 male mice were divided into cuprizone only (Cup-O), cuprizone housed in EE (Cup-EE) and control groups (9 to 10 per group). Environmental enhancement continued for a period of nine weeks. Neurobehavioral tests were conducted after a six-week period of 0.2% cuprizone-enriched diet. All mice were assessed for cognitive performance in the Morris water maze, motor function in rotarod and exploratory behavior in open field test. Results: Cup-EE performed significantly better in fields of spatial learning and memory and motor functioning when compared to Cup-O as evident by Morris water maze (p<0.001) and rotarod (p<0.05) results. Open field test results failed to show an anxiety-like behavior in cuprizone mouse model. Conclusion: Environmental enhancement can improve MS-associated cognitive and motor deficits. Insights gained from these results facilitate the exploration of non-medical modes of intervention as an emerging adjuvant therapy in MS.

Biography:

Dr. Wang is Director of Neuroapoptosis Drug Discovery Laboratory, Department of Neurosurgery, Brigham and Women’s Hospital/Harvard Medical School. Dr. Wang received her PhD from Hebrew University of Jerusalem. She did her postdoctoral training at University of Michigan and Harvard Medical School. Dr. Wang has published about 80 peer-reviewed articles and has served as the Guest Editor, Executive Associate Editor-in-Chief, Handling Editor, and Editorial Board Member for a number of peer-reviewed journals, as well as the scientist reviewer for institutes or foundations including NIH, DOD, BSF, and others, and invited reviewer for 41 peer-reviewed journals.

Abstract:

Inappropriate activation of the cell death program drives the progression of amyotrophic lateral sclerosis (ALS) and Huntington’s disease (HD), as well as increases damage from ischemic stroke. Pharmacological and genetic interventions that inhibit caspases have been shown to slow neurodegeneration in animal models of these chronic illnesses and to lessen the impact of acute brain injury. As in other cells, most physiological pathways leading to cell death include changes in the integrity of mitochondria. Release of mitochondrial cytochrome c into the cytoplasm, often as a consequence of the mitochondrial permeability transition, links upstream events in cell death pathways to activation of capsases that ultimately destroy the cell’s vital structures. Consequently, blocking the release of mitochondrial cytochrome c is the promising strategy to prevent the pathological death of motor neurons, striatal and cortical neurons that cause ALS, HD, and brain injury. We have selected several promising compounds for their ability to prevent cytochrome c release from mitochondria in cultured neurons, drug candidates including melatonin, N-acetyl-L-tryptophan, and N-acetyl-serotonin. Subsequent experiments have shown that these potently neuroprotective agents all exhibit anti-apoptotic activity when used to treat cultured neurons and that they decrease the impact of ALS in mSOD1G93A transgenic ALS mice, or HD in R6/2 transgenic strain whose syndrome resembles HD, or the middle cerebral artery occlusion (MCAO) in C57BL/6 mice that models stroke. The findings may suggest these therapies to be tested in human ALS, HD or stroke patients.

Biography:

The pathogenesis and management of intractable epilepsy (IE) remain a challenge to neuroscientists even today. Electrical stimulation techniques like vagal nerve and deep brain stimulations have assumed significant role as adjunctive therapies. The author postulates pedunculopontine nucleus (PPN) stimulation as an adjunctive therapy in IE, essentially based on the strong antiepileptic property of rapid eye movement (REM) sleep controlled by acetylcholine neurons (AChN) in the PPN, the stimulation of which is found to induce and enhance REM sleep. Even the severe EEG abnormalities (hypsarrhythmia) in West syndrome (WS) disappear during REM sleep; furthermore, in autopsy examination of cases of WS, the number of AChN in PPN in particular have been found to be reduced with relative preservation of other neurons, suggesting a specific involvement of AChN in epileptogenesis. Adrenocorticotrphic hormone is believed to decrease intractable spasms in WS not only through hypothalamo-hypophyseal-adrenal axis but also through a direct action on the pontine tegmentum probably via REM sleep and the anticonvulsant, lamotrigine, is also found to block alpha4beta2nAChRs-mediated currents. Therefore, PPN stimulation is postulated for inducing and enhancing the genesis of REM sleep throughout the night sleep time that is composed mainly of non-rapid eye movement fraction during which the susceptibility to seizure generation and occurrence is known to be enhanced. Involvement and functioning of the PPN in locomotion have formed the basis of its stimulation in controlling gait impairment in Parkinson’s disease. Based on the novel technique, a patent-application has been filed in the United States Patent and Trademark Office.

Abstract:

The pathogenesis and management of intractable epilepsy (IE) remain a challenge to neuroscientists even today. Electrical stimulation techniques like vagal nerve and deep brain stimulations have assumed significant role as adjunctive therapies. The author postulates pedunculopontine nucleus (PPN) stimulation as an adjunctive therapy in IE, essentially based on the strong antiepileptic property of rapid eye movement (REM) sleep controlled by acetylcholine neurons (AChN) in the PPN, the stimulation of which is found to induce and enhance REM sleep. Even the severe EEG abnormalities (hypsarrhythmia) in West syndrome (WS) disappear during REM sleep; furthermore, in autopsy examination of cases of WS, the number of AChN in PPN in particular have been found to be reduced with relative preservation of other neurons, suggesting a specific involvement of AChN in epileptogenesis. Adrenocorticotrphic hormone is believed to decrease intractable spasms in WS not only through hypothalamo-hypophyseal-adrenal axis but also through a direct action on the pontine tegmentum probably via REM sleep and the anticonvulsant, lamotrigine, is also found to block alpha4beta2nAChRs-mediated currents. Therefore, PPN stimulation is postulated for inducing and enhancing the genesis of REM sleep throughout

Biography:

Dr Harinder Jaseja has worked as Professor in Physiology in G R Medical College, India and is presently consultant to Vellore EEG Center, Gwalior, India. Ranked Second in Epilepsy Research in India, he has published novel guidelines for management of patients with cerebral palsy. He has also published pedunculopontine nucleus stimulation (PPNS) as a novel adjunctive therapy and an innovative strategy for selection of deep brain stimulation parameters (DBSPs) in patients with intractable epilepsy. He has filed patent applications separately for PPNS and DBSPs selection-mode. He has published more than 70 international papers and is member of several editorial boards.

Abstract:

Deep brain stimulation (DBS) of anterior thalamic nucleus (ATN) is establishing as an effective adjunctive therapy for patients with intractable epilepsy (IE) not suitable for epilepsy brain surgery and/or vagal nerve stimulation. The judicious selection of DBS parameters (DBSPs) plays a crucial role in the success of ATN-DBS. Conventionally, DBSPs are selected by trial and error requiring multiple sessions and hospital visits warranting a strong need for optimization of the DBSPs with objective assessment of its effects. The author presents an EEG-guided novel and superior approach to the selection of effective DBSPs targeted to induce EEG-desynchronization, which is known to exert potent antiepileptic influence with possibly possession of an additional anti-kindling effect that can suppress or even arrest the ongoing process of epileptogenesis in the patients with intractable epilepsy in addition to exercising control over the intractable seizures. It is further claimed that the innovative EEG-guided approach can successfully optimize the DBSPs resulting in (a) minimum sessions of DBSP adjustments reducing the frequency of hospital visits (b) minimum side effects and (c) minimum consumption of the device battery thus prolonging its life. Preliminary results of the clinical application of the novel approach in the selection of the DBSPs in a small case series have been very promising and encouraging despite which it is strongly recommended that well designed large sized studies are required for its validation and successful clinical outcome. An application for patenting the novel approach has been filed in the United States Patent and Trademark Office.

Biography:

Syeda Nadia Nadeem is 24 years old and completing final year of medical school at University of Liverpool. She is has a strong interest in neurology, especially stroke medicine and most recently worked alongside acclaimed stroke consultants at the Walton Centre, Liverpool. She is also a representative of the Neurology Society in Liverpool and has taught numerous medical students on the topic of stroke and neurology .

Abstract:

Background: Acute ischaemic stroke is the second leading cause of death worldwide. It creates a massive burden not only on the patients’ life but society as a whole. There has been many advancement in stroke management over the past few decades but 2015 has shown giant leaps in this. Up till now, thrombolysis was the main stroke treatment but recently several randomised controlled trials have emerged to demonstrate the efficacy behind using thrombectomy and how it will lead us into the future by treating ischaemic stroke quicker and more effectively than ever before. Aim: To perform a systematic review of the new trials, which compare thrombectomy to best medical care. Furthermore, to critically analyse the current thrombectomy guidelines across UK and Europe in order to develop a thrombectomy best practice protocol, which can be used as a guide worldwide. Method: Numerous articles which highlight the use of thrombectomy compared to thrombolysis alone in acute ischemic stroke were reviewed. Most recent UK and Europe guidelines for thrombectomy use were compared and critically appraised. Results and Conclusion: Results show that thrombectomy used with thrombolysis reduces mortality rates, and improves patients’ functional independence and vessel reperfusion rates significantly from 37% to 100% compared to thrombolysis alone. Current European recommendations complies with these results and forms relevant guidance, whereas, the UKs guidelines are incompatible, lacking structure and recent evidence. As a result, this review has created a new protocol which encompasses the trial results and European recommendations, in the hope to assist physicians worldwide.

Biography:

Abstract:

Forty-two albino male rats aged between 30 and 40 days (weighted 200 g to 250 g) were used in the present study. The left sural nerves of 36 rats were subjected to crush injury at 1 to 6 weeks intervals using 6 animals at each interval. The right and left sural nerves of the rest 6 rats were used as a control. After 2 weeks of the crush injury, the endoneurium showed channel-like spaces that were lined by the collagen bundles with fibroblast-like cells processes. These channels contained degenerated myelin and were connected with the subperineurial spaces. Some of the flattened fibroblast-like cells were arranged in several layers in the subperineurial space, forming barrier-like cellular sheets localizing the endoneurial edema in these spaces. Fibroblast-like cells also wrapped the regenerating nerve fibers by their branching cytoplasmic processes. At the end of the third week, the flattened fibroblasts formed nearly continuous sheets in the subperineurial space. Macrophages were frequently noticed between these cellular barrier-like sheets and in the subperineurial and perivascular spaces. Conclusion: it could be concluded that the endoneurial fibroblast-like cells form barrier-like cellular sheets that localized the endoneurial edema in the subperineurial space and create also the endoneurial channel-like spaces containing degenerated myelin and endoneurial edema helping the resolution of such edema.

Biography:

Dr. Ferrari graduated with honour in Biological Sciences (BSc) and in Experimental and Applied Biology (MSc); she earned the PhD in Biomedical Sciences and is Researcher at Laboratory of Pharmacology and Molecular Medicine of Central Nervous System (CNS). Dr Ferrari’s researches are about CNS Physiopathology and Pharmacology: (a) the study of drugs’ interference on the energetic state of cerebral tissue in healthy and physiopathological experimental conditions, like physiological aging and cerebral ischemia and recovery; (b) Molecular Medicine and Functional Proteomic clinical studies on patients with a diagnosis of Cerebral Ischemia; (c) experimental studies of pharmacological effects of antidepressants on brain energy metabolism. This scientific research activity is documented by 36 publications (IF about 46.5).

Abstract:

Stroke is the third cause of death worldwide and the main cause of chronic, severe adult disability. The current therapy aims at restoring cerebral blood flow within a narrow time window in order to prevent damaging the penumbra which surrounds the infarct core. Intravenous thrombolysis remains the fundamental treatment worldwide, though not ideal for various restrictions and complications limiting to 10% or less the percentage of patients treated within the appropriate time window. Neuroprotection is an alternative or adjunct approach to thrombolysis, targeting cerebral parenchyma in the acute ischemic phase. In the past decades, the efficacy and safety of numerous candidate neuroprotective agents were shown in various animal stroke models. However, in clinical trials, promising pre-clinical studies have not been translated into positive outcomes. Our study analyze the possible reasons for this failure and the new approaches and recommendations to overcome it, as well as novel strategies targeting additional events in ischemia cascade. Finally, the neurorepair strategy will be described with special emphasis on the role of cell-based therapies and ischaemic conditioning.

Biography:

Abstract:

Background and Objective: Depression is a common disabling symptom of multiple sclerosis (MS) with a lifetime prevalence of 50%. The aim of this study is to investigate the impact of induced depression on cuprizone mouse model of demyelination. Methods: Mice were divided into cuprizone with no intervention (Cup-O), cuprizone undergoing induced depression (Cup-Dep) and control groups (9 to 10 per group). Depression was induced by repeated open-space forced swim and was implemented 6 days prior to the testing period. Multiple sclerosis was induced by continuously feeding six-week-old C57BL/6 male mice a 0.2% cuprizone-enriched diet. Spatial learning and memory were tested using Morris water maze while rotarod was used to assess motor function. Results: Cognitive and motor deficits were established in cuprizone mouse model of demyelination as Cup-O had worse results than control group in Morris water maze (p<0.001) and rotarod (p<0.05). Induced depression was seen to exaggerate the aforementioned deficits; Cup-Dep showed a significantly declined performance in Morris water maze (p<0.001) and rotarod (p<0.05) in comparison to Cup-O. Conclusion: Depression can further worsen the natural disease course of MS model. Therefore depression-ameliorating measures should be considered as a part of MS management plan based on the results of this study.

Biography:

O. Nuri Ozgirgin is involved in Otology and Neurotology. Currently being the President of European Academy of Otology and Neurotology. His interests are particularly on Vestibular Medicine. He is the Chairman of the Vertigo Academy International and Editor in Chief of the Journal of International Advanced Otology.

Abstract:

Vestibular diagnosis becomes a challenge for many cases. Even the patient history maintains the basic and most important part of diagnosis, we still need further tests. Understanding and evaluating the vestibulo-ocular reflex added considerably to correct diagnosis. Before the application of sophisticated examinations, evaluation of nystagmus, in the Office or bedside gives important clues. However, we shall need sophisticated tests fort he final diagnosis in some cases. Following evaluation by videonystagmography techniques, inclusion of video head impulse tests, vestibulo-evoked myogenic responses will create a new dimension. Within this lecture new techniques of vestibular evaluation methods will be emphasized.

Biography:

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Abstract:

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Biography:

James Gratwicke qualified in Medicine from the University of Oxford and undertook Post-graduate training in Neurology at the National Hospital for Neurology and Neurosurgery in Queen Square, London. He is a practicing neurologist both at NHNN, Queen Square and St. George’s Hospital in South London, with specialist interests in movement disorders, dementia and neurodegenerative diseases. He is concurrently completing a PhD at UCL’s Institute of Neurology where he works within the Unit of Functional Neurosurgery, delivering both a specialist academic and clinical DBS service to patients. He has published a number of highly cited papers in reputed journals discussing cognitive network dysfunction in dementias and the use of cognitive neuro-modulation as a therapy to counter this.

Abstract:

Dementia remains one of the major challenges facing western society with an estimated affected people of 80 million by 2040. Despite this, only a handful of modestly effective symptomatic therapies exist. Recent trials of pharmacologic agents aimed at reducing aggregation of pathogenic proteins have proved ineffective, likely because of the heterogeneity of the genetic and molecular pathology underlying dementia syndromes and therefore, there is a need for novel approach. Brain stimulation therapies can avoid these difficulties by modulating the disease process downstream at the neural network level, aiming to restore cognitive processing patterns and thereby relieve symptoms. In this presentation, I will discuss how improved understanding of cognitive brain networks are harnessed for development of novel brain stimulation therapies for dementia, with a particular focus on the use of deep brain stimulation. I will cover both basic scientific and clinical aspects of this approach, and discuss the results of two clinical trials recently completed in our unit. I will also look to the future and discuss how cognitive neuro-modulation can be advanced further through improved understanding of brain functioning, from both empirically driven and computationally driven approaches

Biography:

Sybille Krauß studied Biotechnology at the Technische Fachhochschule Berlin until 2002. As a graduate student, she worked at the Max Planck Institute for Molecular Genetics and received her PhD in 2005. After this, she conducted research as Post-doc at the Charité in Berlin in the group of Prof. Susann Schweiger. Since 2010 she is group leader at DZNE in Bonn.

Abstract:

Polyglutamine diseases are monogenic diseases that are caused by elongation of CAG repeat motifs translating into elongated polyglutamine (polyQ) stretches on the protein level. Aggregation of polyQ proteins in the central nervous system of patients is a hallmark of polyQ diseases. Based on the neurotoxic function of these proteins produced from expanded CAG repeats, a reduction of these proteins will be beneficial in the disease context. In line, reduction of polyglutamine protein in disease models for polyglutamine diseases improved the disease phenotype. But how is the protein synthesis rate from expanded CAG repeat mRNAs regulated? One mechanism that we have recently identified to play a role in regulating the translation of huntingtin (HTT) mRNA with expanded CAG repeats involves the MID1-PP2A complex. Mutant HTT mRNA binds to a protein complex containing the MID1 protein, the catalytic subunit of protein phosphatase 2A (PP2Ac), and 40S ribosomal S6 kinase (S6K) in a CAG repeat length-dependent manner. Strikingly, binding of the MID1 protein complex to mutant HTT mRNA, results in an increased translation and subsequent aggregation of mutant HTT. Interestingly, this sequestration of MID1 to expanded CAG repeats does not seem to be limited to mutant HTT mRNA, but is also seen on other mRNAs with expanded CAG repeats such as mutant ATXN3. This makes the MID1-RNA-protein complex a very interesting target to prevent formation of pathological accumulations of mutant polyQ protein in polyQ disorders.

Biography:

Nkemamaka Okonkwo is a Junior Doctor embarking on her Core Medical Training (CMT) in NHS England. She completed her Foundation Training in various trusts across London's North East Thames Deanery and Wales Deanery. Prior to the this, she led student committee projects in conjunction with the Wales 1000 Lives Campaign and the Institute for Healthcare Improvement (IHI) where she is an accredited leader. She supported and pioneered work on issues related to quality improvement and assurance, patient safety and use of retrospective measurement data, real-time monitoring and patient stories to drive overall healthcare improvement.She obtained her medical degree from Cardiff University, an intercalated BSc from Leicester University and is currently studying for an MSc in International Health Management from Imperial College London, where she chairs the BioPharma and Healthcare society.

Abstract:

Background: Temporal artery biopsies (TAB) are often performed in suspected cases of sight-threatening arteritis. The results of which often do little to change clinical management. While the American College of Rheumatology (ACR) formed a clinical classification criterion in 1990 for diagnosing GCA to ensure early steroid therapy was commences, they acknowledge TAB should aim in establishing a definitive diagnosis Aims: The audit aimed to assess if TABs were performed in accordance with the national ACR guideline and whether their results altered course of treatment in suspected GCA. Method: A retrospective audit of all patients undergoing TAB at a single DGH between 2010 and 2014, identified from the histopathology database. Main outcome measures included clinical profile and biochemical criteria associated with positive histology; proportion of negative histology patients who were commenced on steroid therapy; Length of TAB’ relationship between ACR score and TAB result Results: Forty TABs were performed (male: female 1:2, mean age=70.23 years). Three (7.5%) biopsies were histologically positive and 37 (92.5%) were negative. One biopsy was non-arterial. 62.5% of Tabs were performed within the recommended one week of suspected diagnosis. Only 46% of TABs were >1cm. Preoperative steroid therapy was commenced in 80% of patients and a negative histology changed management in 32%. 67.5% had sufficient clinical features to classify GCA and not warrant TAB. Histologically positive TAB patients had higher average age, higher ESR, longer biopsy length and shorter time interval between diagnosis and procedure compared to histologically negative TABs. Conclusion: Raised ESR and higher age may be the most useful diagnostic adjunct of GCA. Many histologically negative TAB individuals were nevertheless clinically diagnosed and managed as GCA. Sub-optimal specimen length may be contributing to lack of diagnostic accuracy. Alternative techniques may be warranted in the near future.

Biography:

Deepa Rani has been working as community health worker and site investigator in Haryana, India for last 3 years. While working in the community, she joined NMP Medical Research Institute and been heading Institute's program as part of lifting the burden compaign, Global Campaign to reduce the burden of headache disorder. She is certified research associate on a multicenteric research study in northern states of India.

Abstract:

Worldwide, headache disorders are among the most common medical conditions.Many people with headache need not experience further pain if the diagnosis and treatment are correct. Most patients do not have correct diagnosis and treatment. This study tested a model for treatment of people with headache disorders at primary health-care level in rural areas of Haryana, India. METHODS: A quasi experimental study with peer education intervention was conducted in selected primary care health clinics. Threee hundred sixty patinets from randomly selected communities of Kaithal, Haryana were assessed through screening questionnaires conducted in pre- and post-intervention periods. Pertinent data on socio-demographic and headache related factors were collected. The statistical packages used for data entry and analysis were epi-info version 3.5.4 and SPSS version 20.0 respectively. RESULTS: When the pre and post intervention data of each group were compared, comprehensive Knowledge of headache (P-Values =0.004) and willingness to go to neurologist for diagnosis and treatment (Pvalue = 0.001) showed significant differences among intervention group during post intervention period. In 68% of patients who completed 12 months' treatment, headache frequency was decreased by at least 60%, and a third of patients were headache free. Medication was well tolerated and reported adverse events were mild; only 36 patients (1%) discontinued medication because of side-effects. CONCLUSION: This study confirmed that this simple protocol was suitable for the treatment of headache disorders in rural areas of India. Physicians and community workers with basic training could diagnose and refere headache patients, with beneficial effects for most patients with treatment.

Biography:

Abstract:

The problems of development of infants‘ brain are known to be complex and urgent because the success of solving these problems increases quality of life in childhood and adolescence. One of these problems is epileptic encephalopathy (EE) in infants. There is a wide variety of this syndrome, what makes the diagnostics very difficult (West, Lennox-Gastaut syndrome (LGS) etc.). The main role in establishing of diagnosis plays EEG with video monitoring that shows hypsarrhytmia of the waves. However, the clinical course in combination with hi-tech examination are strongly recommended. The aim of investigation was optimization of methods of treatment of pharmacological resistant forms of epilepsy that can be illustrated by the case of the two-year boy with symptomatic Lennox-Gastaut syndrome. Materials and methods: The diagnosis was based on the routine examination and clinical manifestations (seizures, appeared with different periodicity). The child was ill since birth and treated with different combinations of antiepileptic drugs (AED). The treatment was unsuccessful, what forced us to find another approach. Tablets of hydrocortisone were prescribed in the start dose of 1.0 mg per 1 kg of body weight (according to professor Olivier Dulac’s scheme), followed by decreasing of dose up to 2 mg. The treatment was carried out during five months. EEG with video monitoring was carried out during 8 hours in active and passive wake, night sleeping and after awaking. Results: First EEG examination provided, when child was 1 year old, showed “sharp slow wave”, “spike-, polyspike-and-waves” complexes in the right parieto-temporal area. In the left one were registered “sharp slow wave” and “spike-and-wave” complexes with reverse of phase under the electrodes P3 and T5. Physiological patterns of sleeping were weakly manifested and periodically were substituted by epileptiform activity. In the middle of therapeutic course the child became seizure-free and considerable more active and some life skills developed. During the one-year follow-up period was not revealed any seizures, though the child did not take AED or hormones. EEG registered just single complexes “sharp slow wave” with amplitude up to 100mcV in left temporal area of the brain with reverse of phase under the electrodes T3, T5. There were not any pathological movements during the sleeping. As result of a treatment was also observed obvious development of child’s brain, which was manifested in physical and mental activity. Conclusion: Thus, we can conclude that early beginning of individually selected therapy in infants with EE and LGS gives the possibility for the normal development of their brain that may be seen in the normalization of physical and mental development.

Biography:

Dr Syed Mohammad Abbas Zaidi completed BUMS and MD (Unani) from Hamdard University, New Delhi. Currently he is working as Assistant Professor at H.S.Z.H. Govt. Unani Medical College, Bhopal. He has published 17 papers in various International/National journals, presented 5 papers abroad (USA, Iran, Malaysia, Japan and Srilanka), many papers in various national conferences across the country and got best paper award in Malaysia in 2011. He has 3 patents and is Associate member of Japan Neuroscience Society, member of editorial board of Indian Journal of Unani Medicine, referee of 3 international journals and member of ethical Committee, Clinical Research Unit, CCRUM, Bhopal.

Abstract:

Delphinium denudatum Wall. (Ranunculaceae) is an indigenous medicinal herb popularly known as ‘Jadwar’ widely used in traditional Unani system of medicine for the treatment of a variety of human ailments including epilepsy. In order to increase the bioavailability, the nanophytosome of the Delphinium denudatum root aqueous fraction (DNP) was prepared, characterized and evaluated. The phospholipid complex of the obtained aqueous fraction (AF) was prepared with Phospholipon 90H. The size of nanophytosomes was determined by dynamic light scattering. HPTLC fingerprinting of the AF was also performed. PTZ and ICES models were used to evaluate the anticonvulsant activity while Rotarod test, Elevated Plus maze test, and Forced swimming test were used to evaluate other neuropharmacological effects at dose level of 400mg/kg and 800mg/kg p.o. The particle size of the prepared DNP was around 500 nm. The DNP exerted significant anticonvulsant activity as compared to control, aqueous fraction and placebo treated groups (p<0.001). The DNP significantly increased the threshold current and decreased the mortality percentage against electroshock at all the doses as compared to control, conventional extract and placebo treated groups. However, there was a significant dose dependent reduction in the recovery period following the convulsions (p<0.001). DNP also exhibited anxiolytic and antidepressant activity in a dose dependent manner. Furthermore, DNP did not cause any evidence of neurotoxicity till dose of 2000 mg/kg p.o. It can be hypothesized that DNP may have better access to the brain as evidenced by its improved efficacy than pure aqueous fraction.

Biography:

Mirjana Djukic has completed her PhD in 2001 at the Faculty of Pharmacy at the University of Belgrade. She became a full professor of Toxicology in 2012. Her research interest has focused on free radicals-mediated mechanism pathways of drugs/poisonings. Accordingly, on oxidative stress-related topics she introduced an optional subject in the faculty study program (2008); wrote (author and editor) two books; published/presented cc 190 papers and has been reviewing articles to reputable journals. She spent two years in the Center for Free Radical and Antioxidant Health (prof. Valerian Kagan lab) at the University Pittsburgh, USA (2002/3, 2010/11).

Abstract:

Paraquat (PQ) neurotoxicity has not thoroughly investigated. Red-ox metabolism of PQ2+ results in superoxide anion radical (O2•) formation. Consequent free radical reactions escalate due to stable resonance radical structure (PQ•+). The OS/NS-associated neurotoxic pathways of PQ were investigated in striatum of Wistar rats after single intrastriatal administration of PQ+ and applied pretreatments, including: N-nitro-L-arginine-methyl ester (L-NAME); 2-amino-5-phosphonovaleric acid (APV); glutathione reductase (GR); and naloxone. Reversible Parkinson’s disease symptoms were observed in PQ group. Contrary to PQ, APV+PQ and GR+PQ groups, initially high O2• reached the normal values in L-name+PQ and naloxone+PQ groups, on 7th day. Superoxide dismutase (SOD) activity declined in L-name+PQ, naloxone+PQ and APV+PQ groups. Initially low SOD activity reached normal values on 7th day in Pq and GR+PQ groups. Lipid peroxidation was the highest in PQ, L-name+PQ and GR+PQ groups. Glutathione (GSH) depletion was considerable in L-name, APV and naloxone pretreated rats across the time. Increased GSH values were achieved in PQ and GR+PQ group on the 7th day. Glutathione peroxidase (GPx) activity was inhibited by GR (within 24 hours) and naloxone; elevated GPx activity declined with the time in APV+PQ and L-name+PQ; while it was high in PQ group until the 7th day. In conclusion, inhibitors of NO-synthase, N-methyl-D-aspartate (NMDA) and opioid receptors, reduced SOD and GPx activities and depleted GSH. Rise of O2• occurred in APV and GR pretreated groups (twice higher than in PQ group), on 7th day, although APV did not influence LPO.

Biography:

Guy H Fontaine has made 15 original contributions at the inception of pacemakers since early 60s. He has serendipitously identified Arrhythmogenic Right Ventricular Dysplasia in the late 70s. He has published more than 900 scientific papers including 201 book chapters. He was the reviewer of 17 journals in Clinical and Basic Science. He served during 5 years as a Member of the Editorial Board of Circulation. He has been invited to give 11 master lectures of 90 minutes each during three weeks in the top universities of China (2014).

Abstract:

Objective: The purpose of this work was to confirm on a pig model, the previous work performed on a rabbit model (ReSS 2012) to demonstrate induction of both brain and general hypothermia used for the first time in OHCA patient. Material & Method: 8 Landrace pigs 39.4±3.9 kg (mean±SD) were studied under general anesthesia according to the WICCM protocol. Temperatures were measured by thermocouples every minute after each injection: Close to the injector inserted up to the nasopharynx without contact to the posterior wall, in the retrograde jugular vein, in the tympanic area, in the esophagus and in the rectum. After stabilization of temperatures, CO2 regulated at 580 psi (40 bars) was delivered for periods of 10 min. A valid data were obtained from 14 injections. We compared the drops in temperatures recorded until stabilization. In these pigs 2±1.5 injections of CO2 were delivered. In a comatose patient successfully defibrillated CO2 was injected in the fossa nasalis from a bottle of 867ml at 580 psi. Results: The initial 90% drop in temperature was detected after 4.7±1.4 min for tympanic and 9.4±4min p=0.02 for the core temperature. Temperatures recorded from the tympanic/jugular probes were identical P=1. Return to stable temperature was observed in 10-15mn. Esophagus drop in temperature was 23±10°C n=6. The drop in temperature was significantly higher in the tympanic area 0.69±0.4 °C than in the core temperature 0.36±0.15 P=0.02.The amount of extracted calories was 14.9±6.7 kilocalories. The patient recovered with absolutely no neurologic deficit despite 6mn of no flow (1224 calories extracted). Discussion: Core temperature drop was similar to that reported in pigs after nasopharynx PFC evaporation. In our experiments the lowest temperature (-30°C) was recorded, as expected, at the exit point for the gas. Significant decrease in temperature of 26°C in the esophagus was always observed. The patient was treated by pure chance but the result was impressive. Conclusion: This study confirms that CO2 expansion in the nasopharynx is effective for brain and body hypothermia in a pig model and in a fortuitous patient. This new technique which is simple, inexpensive and easy to use opens new vistas for the treatment of OHCA and Stroke which, mixed with oxygen, can be started in comatose patient even before CPR or thrombolysis.

Biography:

Professor Geoffrey Burnstock completed his PhD at King's College and University College London. He was head of the Department of Zoology, Melbourne University (1964-1975) before moving to London to head the Department of Anatomy and Developmental Biology, UCL until 1997. He is currently President of the Autonomic Neuroscience Centre, University College Medical School, UK. He is a Fellow of the Australian Academy of Sciences (1971), Royal Society (1986) and Academy of Medical Sciences (1998). He was awarded the Royal Society Gold Medal (2000) and has over 1520 publications and an h-index of 135.

Abstract:

The concept of purinergic neurotransmission (i.e. neurally released ATP acting as an extracellular signalling molecule) was proposed in 1972(Burnstock, 1972). Later it was recognised as a cotransmitter in most, if not all, nerves in the peripheral and central nervous systems, acting on post- and also pre-junctional membranes, at autonomic neuroeffector junctions and ganglionic and central synapses. ATP and its breakdown product adenosine also act as trophic factors during development and regeneration. Brief background information is given about ATP storage, release and ectoenzymatic breakdown. Purines and pyrimidines have key roles in neurotransmission and neuromodulation, with their effects being mediated by P1 (adenosine), P2X ion channel and P2Y G protein-coupled receptors. There is coverage of neuron-glia interactions and of purinergic neuroeffector transmission to non-muscular cells. Purinergic mechanisms and specific receptor subtypes have been shown to be involved in pathological conditions, including brain trauma and ischaemia, epilepsy, visceral and neuropathic pain, neurodegenerative diseases associated with neuroimmune and neuroinflammatory reactions, as well as neuropsychiatric diseases, including depression, anxiety and schizophrenia (see Burnstock, 2007). Specific purinergic receptor subtypes, notably A2A, P2X4 and P2X7 are being explored as therapeutic targets for the treatment of these conditions.

Biography:

Abstract:

The Biology of Neurodegeneration program evolved from our laboratory studying the basic biology of neuronal cytoskeletal protein phosphorylation during development and normal function in the adult. To understand the molecular basis of neurodegeneration our major focus has been to study the regulation of compartment-specific patterns of cytoskeletal protein phosphorylation in neuronal perikarya and axons. We have demonstrated that phosphorylation of the numerous acceptor sites on such proteins as Tau and neurofilament are tightly and topographically regulated and generally confined to the axonal compartment under physiological conditions. However, during neuronal insults, it is deregulated induces neuropathology. During our course of studies to understand the biology of this regulation we identified cyclin dependent kinase5 (Cdk5); a neuron specific kinase involved in the nervous system development, function and survival. It was recognized that in neurodegenerative disorders such as Alzheimer’s disease (AD), Parkinson’s (PD) and Amyotrophic lateral sclerosis (ALS) the pathology was characterized by aberrant and hyper activation of Cdk5 and accumulation of aberrantly hyper phosphorylated cytoskeletal proteins in cell bodies, suggesting that topographic regulation had been compromised. This led inevitably into studies of neurodegeneration in cell culture and model mice with emphasis on Cdk5, that targets numerous neuronal proteins including cytoskeletal protein regulation by phosphorylation, which when deregulated, is responsible for the pathology seen in neurodegenerative diseases. In cell systems, neuronal stress leads to deregulated kinases. Recently we have discovered peptides derived from, p35, and a neuron specific activator of Cdk5, which rescue cells in vitro from stress induced pathology. The questions currently being investigated are (1) how is cytoskeletal protein phosphorylation topographically regulated in neurons? (2) What factors are responsible for the deregulation of Cdk5 in neurons? (3) Can mouse models of AD, PD and ALS be treated therapeutically with peptides that inhibit deregulated Cdk5?

Biography:

Prof. G. Nagesh Babu completed his PhD at the age of 25 years from University of Hyderabad, India. He did his postdoctoral studies from University of Connecticut and University of Arkansas in USA. He also held research positions in Nagoya University, Japan, University of Wisconsin, Madison, USA and University of Porto, Portugal. Currently he is working as a Professor in the Department of Neurology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, India. He has published more than 35 papers in reputed journals and has been serving as an editorial board member of International Journal of Neuroscience and Psychiatry.

Abstract:

It is well known that the neurotoxicity effects of Glutamate (L-Glu) involve the activation of glutamate receptors. However, during periods of cerebral ischemia there is also an activation of the Kyneurinine (KYN) pathway of tryptophan metabolism, which generates the NMDA receptor-glycine site antagonist Kyneurinic Acid (KYNA). We studied the effects of pretreatment of peripheral KYN on acute-L-Glu-induced neurotoxicity. NMDA receptors are supposed to play a crucial role in Glutamate (L-Glu) neurotoxicity.To evaluate the effects of the astrocyte-derived tryptophan metabolite KYNA, on L-Glu neurotoxicity, adult male rats were pretreated with KYN which is a precursor of KYNA, at a dose of 30 mg or 300 mg/kg bw i.p., 2 h before administration of a stereotactic L-Glu bolus (1µmole/1µl) administration into the cerebral cortex. Key oxidant and anti-oxidant parameters were estimated in both brain homogenates and isolated cortical neurons. To obtain individual neurons, finely chopped cerebral cortex tissue was treated with dispase (1000 protease units/ml) for 45 min at 370C. Viability test was done by trypan blue and 90% viable population of neurons was obtained. Acute L-Glu administration increased the rate of lipid peroxidation, nitric oxide and decreased key antioxidant parameters such as SOD, catalase, total glutathione and glutathione reductase in brain homogenates. In isolated cortical neurons, we observed increased levels of reactive oxygen species, calcium along with decreased mitochondrial membrane potential. Peripheral loading of 30 mg/kg dose of KYN had no protective effects on L-Glu induced neurotoxicity, but a dose of 300 mg/kg dose prevented the toxic effects following intracortical L-Glu.

Biography:

Mr. A. K. Srivastava is working in the Department of Pharmaceutics, IIT-BHU as an Associate Professor, of Pharmaceutics. He did his B. Pharm and M. Pharm degree from the Department of Pharmaceutics, IIT-BHU, Varanasi. Before joining the academics in the department he has served in Pharma Industry in production. Mr.Srivastava has vast experience of teaching and research. He has more than 30 year of teaching experience. Mr. Srivastava has guided about 80 research Scholars for M. Pharm degree including 3 Ph. D scholars. He has about 35 research papers in national and international research journals of repute. Mr. A. K Srivastava is recipient of Indian Drug Manufacturer Association, Mumbai (IDMA) gold medal as well as gold medallist in B. Pharm and M. Pharm degree course. Besides, he is involved actively in university administration in various capacities. Area of research of Mr.Srivastava is towards oral Drug Delivery under advance drug delivery system.

Abstract:

Development of an effective formulation for Antitubercular Drug (Rifabutin) involves careful optimization of a number of excipient and process variables. Some times the number of variables are so large that even the most efficient optimized designs require a very large number of trials which put stress on costs as well as time. A creative and Hybrid combination of number of design methods leads to a smaller number of trials. This study was aimed at the development of Nano Structured Lipid Carriers (NLCs) by using a combination of different optimization methods. We were screened using for full factorial design for their effects on formulation characteristics like particle size, entrapment efficiency, Zeta Potential, PDI. Few were found to have in-significant effects on the formulation parameters and hence were screened out. Out of the remaining variables it was found that some of these have significant effects on the size of the particles while the other had a higher influence on the entrapment efficiency and other responses. The screened variables were optimized for their effect on size using the Taguchi orthogonal array. The optimized values of the surfactants and lipids were kept constant for the next stage, where the sonication time, phase ratio, and drug: lipid ratio were varied using the Box–Behnken design and response surface method to optimize the entrapment efficiency. Finally, by performing only less number of trials, few variable were optimised for the development of Nano Lipid Carrier for Rifabutin.

Biography:

Dr David Moore is a post-doctoral research fellow at the Department of Pain Medicine, St James Hospital, Dublin and the Institute of Neurotherapeutics, Dublin City University. Dr Connail McCrory is Dean of the Faculty of Pain Medicine Ireland. He is a Primary Investigator at Trinity College Institute of Neuroscience and the Institute of Neurotherapeutics, Dublin City University. He is Senior Lecturer in the School of Medicine, Trinity College Dublin and Director of Pain Medicine St James Hospital Dublin.

Abstract:

Neuropathic pain poses a significant burden on the individual and society, because of a lack of effective pharmacological therapies. Interventional pain therapies may be more effective in a select cohort of patients. Neuropathic pain results from a lesion or disease of the somatosensory system. Traditionally neuropathic pain was attributed to dysfunctional activity and hypersensitivity of the neuron. However a maladaptive immune response is increasingly recognised as contributing to the maintenance of chronic neuroapthic pain (1). Glial cell activation and altered peptide biosynthesis are implicated in the maintence of persistent neuropathic pain. Human data suggests that NGF, VEGF and BDNF play a role here. This neuroimmune process is maitained by cellular and neuropeptide biosynthetic responses which become pathological. Intrathecal opioids and steroids are associated with alterations in cell signalling and the levels of inflammatory mediators at the neuroimmune interface in humans in vivo (2,3). Markers of glial and immune cell activity, up-regulated in neuropathic pain states, are down-regulated in spinal cord stimulator patients (4). Pulsed radiofrequency of the dorsal root ganglion in patients with radicular pain alters CSF lymphocyte subsets and peptide comcentrations (unpublished data).

Biography:

Fabián Nishida, 30 years old, completed his PhD degree in 2014 at the School of Veterinary Sciences, National University of La Plata. He is now doing his posdoc training. His area of expertise is focused on studies of sensory and motor behaviour, histomorphometry and statistical analysis. Publihed several articles in international journals and participated as a lecturer in several training courses of image analysis and immunohistochemistry. He received some grants for young researchers, as well as honours and prices for his research work. He is now forming three PhD students.

Abstract:

Kainic acid (KA) is an analogue of the neurotransmitter glutamate and causes extensive neuronal network damage and early irreversible loss of neuronal activity. The present work was aimed at evaluating motor and sensory performance of rats and analysing morphometric parameters and immunohistochemical reactivity of spinal cord neurons after intraparenchymal KA injection. Animals were injected either with 0.75 mM, 1 mM or 1.25 mM of KA at the C5 segment of the cervical spinal cord. Motor and sensory performance were evaluated at days 0, 1, 2, 3 and 7 post-injection (pi) and compared with those of saline-treated and non-operated animals. Three animals were euthanized at each time point. All KA-treated animals showed a significant impairment at the motor and sensory tests for the ipsilateral forelimb in a concentration-dependent manner in comparison to control groups. Neuronal cell count showed a significant loss of neurons at C4, C5 and C6 cervical segment when compared with those of saline-treated and non-operated animals. The contralateral side of the cervical segments in KA-treated rats remained unchanged. Immunohistochemical technique showed a similar immunoreactivity pattern with those observed in brains of Alzheimer´s diseases patients. Some improvement at the motor and sensory tests was observed in animals injected with 0.75 mM and 1 mM KA. Moreover, a mild increase in the neuronal count at the damaged segments was also recorded. Functional improvements registered in the motor and sensory tests by day 7 pi may be a consequence of a neuron repairing mechanism triggered soon after the KA excitotoxic effect.

Biography:

Abstract:

Mutation is a change in an organism’s genetic composition. It can be cause by some forms of radiation, some chemical substances and viral infection. Mutation can cause neurological disorders when it takes place in either the neurons or other body cells. a) In other body cells. Once mutation takes place, mutant cells are produced. They could either be begnin (non-cancerous) or malignant (cancerous). Whether the mutant cells are malignant or not, the body’s immune system identifies them to be different from the normal body cells i.e, they lack histocompactibility. This identification is made possible by the presence of T-cell epitopes bound to the Major Histocompactibility Complex Class I, found on the surface of cells. Once the T-cell lymphocytes identify a change on the MHC Class I peptides on a mutant cell(s), those cells are identified as antigens and antibodies are released to destroy them. In this antigen identification process, the molecules that are used by these mutants in growth are identified and are also considered as antigens. Usually, these mutant growth-enabling molecules are in many cases identical to the signaling molecules used by nerve and muscle cells in communicating with each other. They include the synaptic plasma membrane channels e.g the voltage gated potassium chanel and also neurotransmitter receptors e.g the nicotinic acetylcholine receptors. Through the specific antibodies of these antigens, the immune system is able to disable or stop this autocrine growth and possible metastasis by impairing these molecules. In doing this however, these antibodies in the blood plasma reach the nervous system and impair synaptic transmission in the CNS and the PNS. These antibodies are pathogenic to nerves in that they cause demyelination, inflammation, scar formation and axonal destruction in their bid to destroy the identified molecular antigens. This neuropathy leads to neuro-degenerative syndromes. This process can take place in the fetus if the mutation takes place in the mother’s body and also if the mutation takes place in the fetus’ body. If mutation takes place in the mother’s body, the antigen specific antibodies may pass through the placenta into the baby’s circulatory and nervous system, causing damage to both the CNS and the PNS. This accounts for congenital nervous disorders like cerebral palsy.b) In neuron cells. Here, mutation causes neuro-degeneration in that, when the immune system is attacking the mutant neuron buds, it ends up damaging the neurons directly. It also impairs transmission molecules, creating neuron impairment. If this mutation is malignant, it furthers neuro-degeneration by ceasing normal centron and axonal function. Also, if this mutation is caused by viral infection, neuro-degeneration can take place in five ways-: 1. Viral neuropathy. 2. Viral neuron reprogramming. 3. Induced neuron malignancy. 4. Neuron sclerosis. 5. Neuron apoptosis / necrosis.

Biography:

Abstract:

Background: Wilson’s disease (WD) is an autosomal recessive disorder of copper metabolism with a worldwide prevalence of one per 30,000. It is caused by homozygous or compound heterozygous mutations in the ATP7B gene. Studying ATP7B function has been always difficult due to the complexity of the large membrane protein. Design and methods: In order to investigate ATP7B nonsynonymous substitutions, we used a computational analysis approach. Specifically, we used SIFT (Sorting Intolerant from Tolerant) and PolyPhen online softwares to predict possible impact of an amino acid substitution on both structure and function of proteins. Protein structural analysis of amino acid variants was performed by Chimera 1.8 and Project Hope. PolymiRTS was used to analyze the SNPs in the 3'UTR region. Functions and interaction of ATP7B with functional similar gene was predicted using Gene MANIA software. Results: We analyzed 5631 Single Nucleotide Polymorphisms (SNPs) from National Center for Biological Information SNPs database, out of which 838 were coding SNPs, 111 occurred in the mRNA 3′ UTR. The nsSNP; rs28942074, rs28942075, rs28942076, rs41292782, rs60003608 and rs60431989 were identified as deleterious and damaging by the SIFT and PolyPhen programs. Five microRNA binding sites were found to be highly affected due to 3′UTR SNPs. Conclusions: This study suggested that R778L, D765N, G943S, T991M, I967F and I1148T variants of ATP7B protein could directly or indirectly destabilize the amino acid interactions and hydrogen bond networks thus explaining the functional deviations of protein to some extent. That can facilitate early diagnosis and treatment of WD.

Biography:

Abstract:

Background: Temporal artery biopsies (TAB) are often performed in suspected cases of sight-threatening arteritis. The results of which often do little to change clinical management. While the American College of Rheumatology (ACR) formed a clinical classification criterion in 1990 for diagnosing GCA to ensure early steroid therapy was commences, they acknowledge TAB should ain in establishing a definitive diagnosis Aims: The audit aimed to assess if TABs were performed in accordance with the national ACR guideline and whether their results altered course of treatment in suspected GCA. Method: A retrospective audit of all patients undergoing TAB at a single DGH between 2010 and 2014, identified from the hostopathology database. Main outcome measures included clinical profile and biochemical criteria associated with positive histology; proportion of negative histology patients who were commenced on steroid therapy; Length of TAB’ relationship between ACR score and TAB result Results: Forty TABs were performed (male:female 1:2, mean age =70.23 years). Three (7.5%) biopsies were histologically positive and 37 (92.5%) were negative. One biopsy was non-arterial. 62.5% of Tabs were performed within the recommended one week of suspected diagnosis. Only 46% of TABs were >1cm. Preoperative steroid therapy was commenced in 80% of patients and a negative histology changed management in 32%. 67.5% had sufficient clinical features to classify GCA and not warrant TAB. Histologically positive TAB patients had higher average age, higher ESR, longer biopsy length and shorter time interval between diagnosis and procedure compared to histologically negative TABs. Conclusion: Raised ESR and higher age may be the most useful diagnostic adjunct of GCA. Many histologically negative TAB individuals were nevertheless clinically diagnosed and managed as GCA. Sub-optimal specimen length may be contributing to lack of diagnostic accuracy. Alternative techniques may be warranted in the near future.

Biography:

Nicoleta Dumitrescu, 2nd year medical student, “Gr. T. Popa” University of Medicine and Pharmacy (UMF), Iasi, Romania, presented papers to several national and international medical congresses and participated to Student Surgical Society Romania workshops. Professor Ion Poeata, MD, PhD, is Vice-president of the Romanian Neurosurgical Society, chief of the Neurosurgical Department “Prof. dr. N. Oblu” Emergency Clinical Hospital, Iasi, coordinator of the Neurosurgical Department, “Gr. T. Popa” UMF Iasi. Luminita Smaranda Iancu, MD, PhD, is Vice-president of the Romanian Microbiology Society, chief of Microbiology Discipline from “Gr. T. Popa” UMF Iasi, and head of Regional Center of Public Health Iasi.

Abstract:

Worldwide are registered annually about 9 million cases of tuberculosis, Romania being the first in the EU, with an incidence of 87 cases /100.000 inhabitants (2013, World Health Organization). Aim: to report a very rare case of a 27 years-old man diagnosed with a cerebral intraventricular tuberculoma, after he had been treated two months for pulmonary tuberculosis with Mycobacterium tuberculosis - negative sputum smear. Case Report: The patient was brought on August 2015 to “Prof. dr. N. Oblu” Emergency Clinical Hospital, Iasi, by his family because of a confusional syndrome, somnolence and sphincter disorders. Cerebral magnetic resonance imaging showed asymmetrical hydrocephalus and a small homogenous enhanced lesion that was located in the lateral right cerebral ventricle and foramen of Monro. A surgical intervention by endoscopic approach was made. A white-yellowish, soft tumor located in the right lateral ventricle and extended into the third ventricle was seen. Cerebrospinal fluid (CSF) examination revealed leukocytes (8 cells/mm3) and intact red blood cells (340 cells/mm3). Histopathological examination of the biopsy showed rare Langhans giant cells, epithelioid histiocytes, and lymphocytes, but no caseous necrosis. A final diagnosis of an early intraventricular tuberculoma was established. The patient's evolution was favorable under the tuberculostatic treatment and corticoids. Conclusions: This case is customized by the acute development of the intraventricular tuberculoma (while the patient had already been treated with tuberculostatic therapy for two months for active pulmonary tuberculosis), low number of white blood cells in CSF, and negative bacterioscopic exam of sputum.

Biography:

Yuanlong Pan completed his BVM from Gansu Agricultural University, P.R. China. Dr. Pan received his PhD in Animal Nutrition from Virginia Tech, USA and PhD in Human Nutrition from UNC-Greensboro, USA. Dr. Pan conducted research in the area of menopause and cognition at Wake Forest University School of Medicine from 1996 to 2000. In 2000, Dr. Pan joined Nestle Purina Research. He has published more than 18 papers, filed 41 patent applications and obtained 10 patents. Recently Dr. Pan won the Academy of Science-St Louis 2016 George Engelmann Interdisciplinary Award for his outstanding achievement in science through collaboration.

Abstract:

Aging has adverse effects on all tissues and organs in humans and animals including dogs and cats. Just like in humans, some of the senior dogs and cats eventually develop cognitive impairment and dementia called cognitive dysfunction syndrome (CDS). Since CDS is not a curable disease, our research has been focused on nutritional solutions that promote healthy brain aging in dogs and cats for the past 15 years. We have developed two solutions to enhance cognitive functions in dogs and cats. The first approach is to address the reduced ability of brain cells to utilize glucose as energy by providing medium chain triglycerides (MCTs), and we have confirmed that MCTs do enhance cognition in aging dogs. The second solution is to minimize known risk factors associated with brain aging. Since there are multiple risk factors, we have developed a nutrient blend and demonstrated its cognition-enhancing benefits in middle-aged and aging cats. In summary, our research shows that optimal nutrition can enhance cognitive functions in healthy aging dogs and cats. What we have learned from pets may be able to facilitate the development of nutritional and therapeutic solutions for people.

Biography:

Abstract:

Aims and Hypothesis: To review the previous case reports on positive anti-NMDAR antibodies that were treated with ECT. Background: It is now well accepted that autoimmune encephalitis can present with a combination of neurological and psychiatric symptoms. Currently, the most widely used therapy for these conditions is prompt plasmapheresis and steroid treatment (and tumour resection if indicated), followed by second line immunosuppression if this fails. Cases: We discuss several case reports, which suggest that ECT plays a role in treatment for some types of autoimmune encephalitis, particularly those in which psychiatric symptoms are especially debilitating and refractory to standard treatment. We present a new case of a 71 year old previously healthy female who presented with depression and anxiety after anti-NMDAR antibodies were isolated, she received plasmapheresis and corticosteroid treatment and then she underwent 8 sessions of ECT and returned to her premorbid state. Discussion: We discuss factors predicting good outcome and possible mechanisms behind the use of ECT in autoimmune encephalitis. Conclusions: Although there are still only a small number of case reports supporting the theory that ECT is effective in treating symptoms of autoimmune encephalitis, it is reasonable to suggest that it should be considered as an alternative or adjunct to standard immunosuppressive therapies.

Biography:

Dr Davide Vito Moretti is consultant neurologist, chief of the clinical neurophysiology service and researcher at the National Institute of Research and Cure for Mental disorders and Dementia S john of God, Brescia, Italy, Professor of neurophysiology at UniLudes University in Lugano. He received his medical degree from Catholic University in Rome and completed his residency in neurology and fellowship in movement disorders at University of Trieste, Italy. Moreover, he received the PhD in neurophysiology at La Sapienza University. Dr Moretti is currently involved in research and care of subjects with Alzheimer's disease and movement disorders in the Alzheimer Operative Unit of the S. John of God Institute.

Abstract:

The increase of EEG upper/low alpha power ratio has been associated to a lower regional blood perfusion, to atrophy of temporo-parietal brain areas, and to reduction of hippocampal volume in subjects affected by mild cognitive impairment (MCI) due to Alzheimer's disease as compared to non converters.Moreover, Also, The EEG theta frequency activity is quite different in the groups. We investigated the correlation between the biomarkers and memory performances.Methods: EEG Alpha3/alpha2 power ratio as well as cortical thickness was computed for each subject has been computed in 74 adult subjects with prodromal AD. In 27 of them underwent also blood perfusion assessment sby ingle-photon emission computed tomography (SPECT) Pearson’s r was used to assess the topography of the correlation between cortical thinning as well as between brain perfusion and memory impairment Results: In higher alpha3/alpha2 frequency power ratio group greater cortical atrophy and lower regional perfusional value in temporo-parietal cortex was found correlated to an increase of EEG theta frequency. Moreover, both in MRI group and in the SPECT MCI group memory impairment was more pronounced Conclusion: High EEG upper/low alpha power ratio was associated with cortical thinning lower perfusion in temporo-parietal. Moreover, atrophy and lower regional perfusional rate were both significantly correlated with emory impairment in MCI subjects. The of EEG upper/low alpha frequency power ratio could be useful for identifying individuals at risk for progression to AD dementia and may be of value in clinical context.

Biography:

Zhu Lei is working for his PhD at the Second Military Medical University. He has published 10 papers in reputed journals .

Abstract:

The aim of this study was to evaluate the feasibility of using the intact S1 nerve root as a donor nerve to repair an avulsion of the contralateral lumbosacral plexus. Two cohorts of patients were recruited. In cohort 1, the L4–S4 nerve roots of 15 patients with a unilateral fracture of the sacrum and sacral nerve injury were stimulated during surgery to establish the precise functional distribution of the S1 nerve root and its proportional contribution to individual muscles. In cohort 2, the contralateral uninjured S1 nerve root of six patients with a unilateral lumbosacral plexus avulsion was transected extradurally and used with a 25 cm segment of the common peroneal nerve from the injured leg to reconstruct the avulsed plexus. The results from cohort 1 showed that the innervation of S1 in each muscle can be compensated for by L4, L5, S2 and S3. Numbness in the toes and a reduction in strength were found after surgery in cohort 2, but these symptoms gradually disappeared and strength recovered. The results of electrophysiological studies of the donor limb were generally normal. Severing the S1 nerve root does not appear to damage the healthy limb as far as clinical assessment and electrophysiological testing can determine. Consequently, the S1 nerve can be considered to be a suitable donor nerve for reconstruction of an avulsed contralateral lumbosacral plexus.