4^th International conference & Exhibition on Neurology and Therapeutics July 27-29, 2015 Rome, Italy

Biography:

Dr. DeFeo is noted as one of the leading experts of the DSM-5 in the State of California. She has conducted over 50 state, national, and international trainings on the topic. Dr. DeFeo was the highlighted presenter at the 18th Annual Inter-national Violence, Abuse, and Trauma Conference (IVAT) in San Diego in September, 2013, the 18th Annual IVAT Conference in Honolulu, Hawaii in March, 2014, and the Illinois American Association for Marriage and Family Therapy Annual Conference in Naperville, Illinois to conduct a full 7 hour workshop to educate Clinical Psychologists, Social Workers, Marriage and Family Therapists, Psychiatrists, and Medical Doctors/Professionals on the DSM-5 and ICD-10 diagnostic systems. Dr. DeFeo’s DSM-5 and ICD-10 training is also an approved accredited workshop with the Association for Advanced Training in the Behavioral Sciences (AATBS) to train social workers, psychologists, psychiatrists, medical physicians, and marriage and family therapists in the United States. Additionally, Dr. DeFeo is working with the Mexican Board of Professionals to institute the DSM-5 into the Mexican Higher Education Institutions, and has presented this topic at the First Annual Psychological Society Conference in Buenos Aires, Argentina in October, 2014 and various locations in Mexico (Tijuana, Ensenada, and Mexicali). Dr. DeFeo presently is a California licensed psychologist, distinguished professor of psychology, and Interim Associate Chair for the Department of Marriage and Family Therapy at the Chicago School of Professional Psychology in Irvine, California where she has been working since 2010. Dr. DeFeo also is a senior reviewer and editor for the Journal of Psychiatry, OMICS, and the Journal of Hispanic Higher Education.

Abstract:

The unfortunate reality exists that there is a significant barrier between neuroscience and psychology. There are over 600 neurological conditions that are recognized and treated in the field of medicine, such as Muscular Dystrophy, Huntington’s Disease, Rett’s Syndrome, Bell’s Palsy, and Locked-In Syndrome to name a few; however, the psychological manifestations and treatments are most often ignored. It is imperative that the field of medicine addresses the reciprocity between neurological conditions andpsychosocial functioning. The goal of this keynote is to educate the audience on how to recognize, address, and provide appropriate therapeutic interventions, both medically and psychologically.

Biography:

Dr. Pant received his M.A. and Ph.D. degrees in Physics from Agra University, Agra, India. His postdoctoral studies were conducted on the mechanisms of electron and ion transport in model membrane systems at the Department of Biophysics at Michigan State University. He joined the Laboratory of Neurobiology in the NIMH as a senior staff fellow in 1974 with Dr. Ichiji Tasaki where he studied the function of the axonal cytoskeleton in the squid giant axon. In 1979 he moved to the NIAAA extending his studies on the neuronal cytoskeleton and the effects of alcohol on its regulation. Dr. Pant moved to the NINDS, Laboratory of Neurochemistry in 1987 where he is presently chief of the section on Cytoskeleton Regulation. His laboratory is studying the mechanisms of topographic regulation of neuronal cytoskeleton proteins by post-translational modification, including the role of kinase cascades in normal brain and during neurodegeneration.

Abstract:

Biological processes are tightly regulated under physiological conditions. Neurobiology occurs upon deregulation of these tightly regulated processes. The Biology of neurodegeneration program evolved in our laboratory studying the basic biology of neuronal cytoskeletal protein phosphorylation regulation 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 (neuronal cell body), axons and dendritic processes. During our studies on the compartment specific phosphorylation of cytoskeletal proteins in the neurons, we discovered a novel kinase, Cdk5, a Cell Cycle dependent like kinase in the brain. Though it binds with cyclins, however, its activity is primarily restricted to neurons due to its binding and regulation by neuron specific proteins p35kDa and p39kDa. Cdk5. By virtue of its tight regulation, multifunctional role in neuronal development, migration, synaptogenesis and survival Cdk5 targets a large number of different types of neuronal processes and has emerged as a major player in nervous system function in health and disease. We have demonstrated that phosphorylation of the numerous acceptor sites on neuronal intermediate filament proteins (NIFPs) as neurofilaments (NFs) and Tau is tightly regulated topographically and generally confined to the axonal compartment. It was recognized that in neurodegenerative disorders such as Alzheimer’s disease (AD) and Amyotrophic lateral sclerosis (ALS), the pathology was characterized by an accumulation of aberrantly and hyper- phosphorylated cytoskeletal proteins in cell bodies, suggesting that topographic regulation had been compromised. Our studies of neurodegeneration in cell culture and model mice with emphasis on a specific neuronal protein kinases, (Cdk5), that targets numerous neuronal proteins including cytoskeletal proteins, which when deregulated, may be responsible for the pathology seen in neurodegeneration. In cell systems, neuronal stress leads to deregulation of Cdk5, accompanied by abnormal cytoskeletal protein phosphorylation and cell death characteristic of neurodegeneration. Recently we have developed peptides derived from, p35, a neuron specific activator of Cdk5, for deregulated Cdk5 activity which rescue cells in vitro from this stress induced pathology and in vivo, in AD, ALS and PD model mice. We have investigated (1) how cytoskeletal protein phosphorylation is topographically and tightly deregulated in neurons? (2) What factors are responsible for this deregulation? (3) And treated mouse models of AD, ALS and PD therapeutically with a small peptide, p5, (24 amino acid) derived from Cdk5 activator protein, p35, that specifically inhibit deregulated Cdk5 (Cdk5/p25) but not the physiological Cdk5 (Cdk5/p35) required for nervous system function. Currently, most therapeutic approaches targeting the deregulated Cdk5 and other kinases in neurodegenerative disorders have focused primarily on drugs like roscovitine that inhibit Cdk5 activity by interfering with the ATP binding domain of the kinases. These drugs, however, lack sufficient specificity, since all the kinases including cell cycle Cdks, are vulnerable at the ATP binding site targeted by these drug molecules. P5 is non-toxic, thus is most suitable therapeutic reagent for AD and other neurodegenerative diseases.

Biography:

Hamed Benghuzzi is currently the Professor and Chairman at university of Mississippi medical center, USA. His area of research is the development and applications of novel ceramic drug delivery systems (over 26 years/over 250 publications and 600 abstracts at various meeting). He was fortunate to be recognized as a fellow by the American Institute of Medical and Biological Engineering, as well as, International Fellow by the World Congress of Biomaterials Societies (Japanese, American, Asian, and European). His passion is teaching and training students. He had been the mentor of several faculty at the school of health related professions and other clinical departments including two orthopedic surgery faculty through grants supported by OTA and OREF. He served and serving as a major advisor for over 30 PhD students as well as a mentor for students at various levels (High school, undergraduate, MS, residents and postdoctoral). He is also a course director for several graduate and undergraduate courses. These include Pathophysiology (I and II), Histopathology, Pathophysiological phenomena, Human Physiology and Pathology. Administratively; he served as a chair for departments of Health Sciences, Cytotechnology and currently he serve as a chair of the Department of Diagnostic and Clinical health sciences and Director of CHS program.

Abstract:

Evaluation of devices, drugs, and drug delivery systems (CDS) have been investigated by both in vitro and in vivo procedures. Ceramic drug delivery systems have shown to be biocompatible, non-toxic and highly acceptable by the host. The CDS can also reduce handling of animals and facilitate long-term evaluations before conducting clinical trials. To date, CDS have been used to deliver various biologicals such aldosterone, androstanedione, beta-lactoglobulin, bovine serum albumin, chymotrypsin, danazol, difluoromeythylornithine, dihydrotestosterone, estradiol, gamma globulin, gonadotrophic releasing hormone, gossypol, growth hormone, insulin, pepsin, progesterone, neuropeptide Y antagonist, thymoquinone, vitamins and testosterone to name a few . The results of ourfindings provided significant scientific evidence to effectively use CDS as an alternative route of drug administration to treat diseases requiring long-term chronic drug therapy as well as disorders caused by deficiency of certain medications (hormone replacement therapy).

Biography:

Alessandro Morelli (b. 1943) has studied enzyme Glucose-6-P-dehydrogenase and its molecular mechanism of senescence. He has been working in the field of phototransducion and molecular events in photoreceptor cells of vertebrate retina. He has discovered the protein FX, a NADP dependent enzyme catalizing synthesis of GDP-L-fucose. He has been working on the effects of electromagnetic fields of extremely low frequency on the activity of enzymes involved in bioenergeticprocess. Recently he has studied the myelin energetic function in brain put in in evidence the ATP extramitochondrial synthesis, with application in the study of Multiple Sclerosis and other neurodegenerative deseases.

Abstract:

A new paradigm other than insulator may arise for myelin, consistent to the fact that myelination is not continuous, as previously thought, and that myelin can aerobically synthesize ATP and deliver it to the axoplasm trough gap-junctions. Myelination is triggered by neuronal activity, which in turn regulates myelin remodeling. It may be hypothesized that after birth, intense firing depletes axonal ATP causing a rise in Adenosine, that triggers myelination (through purinergic receptor signalling): only those neurons which are fed with ATP can survive. Anoxia causes memory loss: i.e. memory requires energy. It may represent a neural network energized by myelination.

Biography:

Dr. Michael Seibenheneris a research Scientist with a strong background in hypothesis development, experimental design and planning. Over 20 years, he have experience in supervision and training of project personnel and extensive bench top research experience in cell and molecular biology. He looking to use knowledge gained over my years of peer reviewed research to further my research career as well as pass on the knowledge He have learned to another generation of scientists. He did his PhD from Auburn University.

Abstract:

Affective spectrum and anxiety disorders have come to be recognized as the most prevalently diagnosed psychiatric disorders, as well as, being intimately associated with neurodegenerative disease. Among a suite of potential causes, changes in mitochondrial energy metabolism and function have been associated with such disorders. Thus, finding proteins that specifically alter mitochondrial functionality is important to identify molecular targets for drug discovery. The scaffolding and mitophagy related protein Sequestosome1 (SQSTM1/p62) is a component of all known aggresomes associated with multiple neurodegenerative diseases. It has also been recognized as playing a role in both basal mitochondrial activity as well as, degradation of defective mitochondria by mitophagy. We have generated a transgenic mouse overexpressing SQSTM1/p62 specifically in the hippocampal region of the brain and have shown increased mitochondrial energy output and improvement in transcription factor import into the mitochondrial matrix. These elevated levels of mitochondrial functionality correlate directly with discernible improvements in mouse behavior patterns related to affective spectrum and anxiety disorders, as well as, improvements in cognition, spatial learning and long term memory formation. With measurable improvements in biochemical function and behavioral patterns, SQSTM1/p62 appears to be a prime candidate as a protein that improves mitochondrial functionality while also improving behaviors related to anxiety and affective spectrum disorders making it a potential biomarker for mitochondrial related neurodegenerative diseases.

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 70 peer-reviewed articles and has served as the Guest Editor, 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 34 peer-reviewed journals.

Abstract:

Amyotrophic Lateral Sclerosis (ALS) is a fatal and rare chronic neurodegenerative disease. Multiple mechanisms proposed as responsible for ALS pathogenesis include mitochondrial dysfunction, apoptosis, oxidative stress, inflammation, glutamate excitotoxicity, and protein degradation. Because riluzole, the only Food and Drug Administration (FDA)-approved treatment, prolongs the ALS patient’s life by only 3 months, new therapeutic treatments that may delay disease onset, slow progression, prolong survival, and ultimately reduce the burden of disease are urgently needed. The impact of various small pharmacological compounds targeting the proposed pathogenic mechanisms of ALS will be summarized. Furthermore, melatonin, an agonist of melatonin receptors, delays disease onset, extends lifespan, and slows progression of mSOD1G93A ALS transgenic mice will be discussed.

Biography:

Dr. Anantha Ramanathan is a Vascular and Endovascular Surgeon at the Central Coast of New South Wales Australia. His niche areas are endovascular surgery, dialysis access and carotid endarterectomy. He special interests are amputation prevention, stroke prevention and creation and maintenance of dialysis access fistulas. He is a fanatic in his belief in limb preservation, preservation of AV fistulas and rapid access carotid endarterectomy. Nowadays it is feasible to treat most critically ischaemic limbs by endovascular techniques. He do not give up until he have exhausted all possibilities of treatment. Hence he believe his amputation rates are low. Similarly he do not abandon failed or failing AV fistulas without trying hard to rescue them. He absolutely committed to his patients. His patients love him. Many patients have commented that "he care." And he smile a lot. Almost every patient who leaves his room leaves with a smile. Vascular ultrasound forms an integral part of his work. He also a conjoint Senior Lecturer at University of Newcastle. He is also an author. He have published an anthology of 80 poems and two novels in Tamil. The English translations of the novels will be published soon. He have won prizes for essay and poetry in English and Tamil. He have published articles, poems and stories in several magazines. He also have many unpublished poems. He will embark on writing my next novel soon.

Abstract:

History: A fit 20 year old male personal trainer presented with a history of hearing a continuous buzzing noise in his left ear for about a month. The noise was present at all times and interfered with his daily activity and sleep. He was otherwise healthy. He could not remember how it started but on being questioned about trauma he volunteered that he was involved in an altercation about a month before, and was punched in the left side of the neck. Though he did not lose consciousness, he had a stiff neck from the next morning for a few days. There was no hearing impairment. Examination: Physical examination revealed that the main abnormality was a palpable thrill and an audible continuous bruit at the apex of the left posterior triangle of the neck, radiating towards the left ear. A diagnosis of AV fistula was made. Investigation: The initial duplex scan and MRI could not demonstrate the AV fistula but a second duplex scan demonstrated high velocity flow in the internal jugular vein (PSV 423cm/sec). The V3 segment of the vertebral artery showed high flow low resistance pattern (PSV 395cm/sec; EDV 175 cm/sec) with a lot of turbulence. A diagnosis of vertebrojugular AV fistula due to blunt trauma was made. The right vertebral artery was normal. Treatment: The condition was treated successfully by endovascular placement of detachable coils proximal and distal to the lesion in the left vertebral artery, with Onyx (TM) injection of the fistula itself. The vertebral artery was sacrificed without any clinical consequences. Discussion: Vertebral artery AV fistulae are rare and usually occur after trauma. The V3 segment of the artery is most at risk as the artery leaves the protective environment of the vertebral foramina to enter the foramen magnum. The artery is relatively superficial in this situation and can be injured. Blunt trauma of the area is the commonest cause. This patient was relatively lucky. In Australia we had a recent high profile sporting tragedy where a young cricketer died after being struck in this region by a cricket ball. In that case the vertebral artery bled inside the cranium, causing rapid decompensation.

Biography:

Dr. Robert D. Dimaio graduated from the Philadelphia College of Osteopathic Medicine in 1985. He works in Pennsauken, NJ and specializes in Family Medicine and Osteopathic Manipulative Medicine. Dr. Dimaio is affiliated with Kennedy Health System Cherry Hill and Our Lady Of Lourdes Medical Center.

Abstract:

Repeated seizures are often associated with development of refractory chronic epilepsy, the most common formof which is temporal lobe epilepsy. G-protein-coupled cannabinoid receptors (CB1 and CB2 receptors) regulateneuronal excitability and have been shown to mediate acute anticonvulsant effects of cannabinoids in animalmodels. However, the potential of cannabinoids to prevent chronic neuronal damage and development ofepilepsy remains unexplored. We hypothesized that treatment with a CB receptor agonist after an episode ofstatus epilepticus – but before development of spontaneous recurrent seizures – might prevent the developmentof functional changes that lead to chronic epilepsy. Using the rat pilocarpinemodel, a therapeutic approach wassimulated by administering the CB agonist,WIN55,212-2 after an episode of status epilepticus. Epileptic behaviorwas monitored during development of spontaneous recurrent seizures for up to 6 months. Histology,neurochemistry, redox status and NMDA receptor subunit expression were assessed at 6 months afterpilocarpine-induced seizures. Sub-acute treatment with WIN 55,212-2 (for 15 days starting 24 h after PILOinjection) dramatically attenuated the severity, duration and frequency of spontaneous recurrent seizures. Further, in contrast to vehicle-treated animals, hippocampi fromWIN 55,212-2-treated animals showed: normalthiol redox state, normal NR2A and NR2B subunit expression, preservation of GABAergic neurons and preventionof abnormal proliferation of GABAergic progenitors. This study shows for the first time that, after a knowninciting event, treatmentwith a compound targeting CB receptors has the potential to prevent the epileptogenicevents that result in chronic epileptic damage.

Biography:

Nathali Kaushansky, PhD, is a staff scientist in the Neurobiology Department at the Weizmann institute of Science. Dr. Kaushansky received her BSc in Chemistry and MSc in Biomedical Engineering from the Technion – Israel Institute of Technology, Haifa, Israel. She completed her PhD studies and post-doctoral training in the Immunology Department in The Weizmann Institute of Science. In the last 10 years Dr. Kaushansky’s work has focused on characterization of autoimmune T- and B-cells against myelin and neuronal target antigens in Multiple Sclerosis (MS). Her study aims to establish a highly specific “multi – targeting” immunomodulatory approach via co-antagonizing of most known and potentially pathogenic T-cell autoreactivities in MS. The primary goals of her recent research were 1: studying mechanisms underlying immunomodulation by this multi epitope targeting agent (specifically designed artificial multi-epitope protein (Y-MSPc)-recently published) and 2: studying immunogenetics of susceptibility to MS, mainly at defining HLA-DR2-related epitopes of the different most important myelin target antigens in MS.

Abstract:

It is now widely accepted that the pathogenic autoimmunity inMS, as well as in other organ-specific autoimmune diseases, can bedirected against several target antigens. We recently showed that a concomitant ‘‘multi-epitope-targeting’’ approach,using a specifically designed artificial multi-epitope protein (Y-MSPc) is required foreffective antigen-based immune-specific therapy of organ-specificautoimmune diseases associated with complex and dynamicpathogenic autoimmunity, such as MS.Y-MSPcwas superior to peptide(s) in concomitantly downregulating pathogenic T-cellsreactivity against multiple myelin antigens/epitopes, via the induction of effective and longer lasting peripheral regulatorymechanisms (cytokine shift, anergy, and Foxp3+ CTLA4+ regulatory T-cells . Moreover, we identified a tolerogenic myeloid DC subset in theCNS and spleen of EAE mice playing an important role in immunoregulation process in EAE, following Y-MSPc treatment . Our results demonstrate that immune tolerance induced by Y-MSPc is associated by increase of CD11c+CD11b+Gr1 myeloid derived dendritic cells in the CNS and spleen. These myeloid DCs exhibited immunoregulatory characteristics, including increased production of IL-4, IL-10 and TGF-b but reduced IL-12. Furthermore, CD11c+CD11b+Gr1 DCs were also capable of inhibiting the proliferation of PLP139-151-specific T cells in vitro and significantly suppressed ongoing EAE upon adaptive transfer. In addition, adaptive transfer of CD11c+CD11b+Gr1 DCs derived from YMSPc treated mice to EAE induced mice resulted in remarkably upregulation of CD4FOXP3 regulatory cells. Taken together, these findings suggestthat i.v.administration of the multi epitope protein (Y-MSPc) results in maintaining peripheral tolerance and reduce EAE incidence by an increase in tolerogenic CD11c+CD11b+Gr1 .

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). Prior to joining NIH in 2012, Dr. Tamiz had held scientific and management positions in research and development of therapeutic programs at Corvas International (acquired by Dendreon), CovX (now part of Pfizer), and Alba Therapeutics. Dr. Tamiz received his Ph.D. at University of Oregon and conducted postdoctoral research at the Department of Neuroscience at Georgetown University Medical Center.

Abstract:

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:

Kaja is an experienced neurobiologist with a long-standing research track record in academia and the biotech and pharmaceutical industry. Kaja currently serves as Associate Director of Preclinical Research at the Vision Research Center at the University of Missouri - Kansas City, School of Medicine. He is the Director of Microscopy of the imaging core facility at the Vision Research Center and also holds an appointment to Assistant Professor of Ophthalmology. His NIH-funded research program focuses on human neurological and neurodegenerative diseases, visual disorders and inflammation. Kaja obtained his B.Sc. (Hons.) degree in Molecular Biology and Biochemistry from Durham University, UK and holds a Ph.D. degree in Medicine/Neuroscience from Leiden University, The Netherlands. Prior to joining the faculty at the University of Missouri - Kansas City, he has performed postdoctoral work at The University of British Columbia (Vancouver, B.C., Canada) and the University of North Texas Health Science Center (Fort Worth, TX). In addition to his academic work, Dr. Kaja has worked and consulted for a number of pharmaceutical companies, incl. Novo Nordisk A/S, Bayer AG, Neuromed Pharmaceuticals Inc., and NeuroSearch A/S. He is CEO and co-founder of K&P Scientific LLC, a scientific consulting company headquartered in Kansas City, MO.

Abstract:

Alzheimer’s disease (AD) is the most common form of dementia, affecting more than 5 mi Americans. As such, AD poses a significant burden on the affected individual, caregivers and society. Most cases of AD are attributed to the sporadic form, which is believed to be of multifactorial origin.However, several genetic loci etiological for the rare familial form of the disease have been identified. One of the loci is the group of presenilin proteins, which form the enzymatic core of the γ-secretase complex. Most of the almost 200 identified familial AD mutations in presenilins are located in the gene encoding presenilin-1, while presenilin-2 mutations typically cause later onset familial AD. Recent evidence identified the group of presenilinproteins as potent modulators of intracellular calcium signaling, through potentiation of the intracellular ryanodine receptor, which likely underlies this phenomenon. This potentiation occurs via the highly evolutionarily conserved N-terminal region of presenilin, resulting in differential modulation of the ryanodine receptor by presenilin-1 and presenilin-2. The proposed mechanism is in accordance with previous studies identifying elevated Ca2+ concentrations in the endoplasmic reticulum during AD, and the critical role of ryanodine receptors in regulating calcium via calcium-induced calcium release. Furthermore, ryanodine receptors contribute to the pathologic, elevated intracellular Ca2+ concentrations observed in AD. Intriguingly, similar Ca2+dyshomeostasis occurs during healthy aging, in the absence of known mutations. Utilizing preclinical models for healthy aging, we have implicated presenilin proteins in the etiology of age-related changes in synaptic signaling and, ultimately, age-related deficits in memory and motor coordination. In this keynote talk I will summarize the evidence for the group of presenilin proteins as a novel class of calcium modulators, and discuss the opportunities for targeting presenilin proteins as novel drug targets for age-related and neurodegenerative diseases, incl. AD. Biography Kaja is an experienced neurobiologist with a long-standing research track record in academia and the biotech and pharmaceutical industry. Dr. Kaja currently serves as Associate Director of Preclinical Research at the Vision Research Center at the University of Missouri - Kansas City, School of Medicine. He is the Director of Microscopy of the imaging core facility at the Vision Research Center and also holds an appointment to Assistant Professor of Ophthalmology. His NIH-funded research program focuses on human neurological and neurodegenerative diseases, visual disorders and inflammation. Dr. Kaja obtained his B.Sc. (Hons.) degree in Molecular Biology and Biochemistry from Durham University, UK and holds a Ph.D. degree in Medicine/Neuroscience from Leiden University, The Netherlands. Prior to joining the faculty at the University of Missouri - Kansas City, he has performed postdoctoral work at The University of British Columbia (Vancouver, B.C., Canada) and the University of North Texas Health Science Center (Fort Worth, TX). In addition to his academic work, Dr. Kaja has worked and consulted for a number of pharmaceutical companies, incl. Novo Nordisk A/S, Bayer AG, Neuromed Pharmaceuticals Inc., and NeuroSearch A/S. He is CEO and co-founder of K&P Scientific LLC, a scientific consulting company headquartered in Kansas City, MO

Biography:

Dr. is a 4th Grade Hebrew/Religious School Teacher in Emanuel Congregation from September 2011 – Present (4 years 4 months)Chicago, IL (Illinois). She teach Hebrew (2nd year) using Mitkadem and CHAI Curriculum and Life Cycle for the 4th Grade! She was an interim Facilities Manager in Emanuel Congregation from March 2013 – February 2014 (1 year)Chicago, IL (Illinois). She maintained the Emanuel Calendar that determines who is where at any given minute in the Emanuel Facility. She also scheduled security on a monthly basis. She was Executive Director in Decalogue Society of Lawyers from March 2006 – November 2008 (2 years 9 months)Chicago, IL. She was an Assistant Property Manager in Wesley Realty Group form 2001 – 2004 (3 years)Evanston, IL. She was Senior Business Consultant in Kraft Foods Group from 1998 – 2000 (2 years)Glenview, IL. She was a PROJECT LEADER/SENIOR ANALYST in CCH Incorporated from 1993 – 1998 (5 years)Chicago, IL

Abstract:

Background: Mild-moderate alcohol intake is widely considered to be associated with decreased risk of developing Alzheimer disease (AD), while heavy drinking increases the risk. There is little information about how alcohol affects the cognitive profile among those already diagnosed with AD. Objective: To examine the relationship between alcohol, both the amount and type, and cognitive decline in a cohort of AD patients. Methods: A cohort of 360 patients with early AD in New York, Boston, Baltimore and Paris were followed-up biannually for up to 19.28 years. At each visit, the cognitive profile of the patients was assessed using the modified Mini-Mental State Examination (mMMSE), and patients’ alcohol intake, including beverage type, was reported by patients’ primary caregivers. General estimating equation analysis was used to determine whether baseline alcohol use was associated with the rate of cognitive decline. Findings: Heavy drinkers (8 or more alcoholic drinks/week) had a faster cognitive decline, deteriorating 2.625 more points on their mMMSE score annually compared to abstainers (P≤0.0001), or 3.429 more points compared to mild-moderate drinkers (1-7 alcoholic drinks/week) (P=0.006). There was no significant difference when comparing mild-moderate drinkers to abstainers. Increasing standard drinks of hard liquor, but not beer or wine, was also associated with a faster rate of cognitive decline (β=-0.165 P=≤0.0001). Conclusions: Heavy alcohol consumption and more hard liquor are associated with a faster rate of cognitive decline in AD patients, suggesting that they may hasten progression of AD. Our results suggest that alcohol drinking habits might alter the course of AD.

Biography:

Abstract:

Purpose Progressive myoclonic epilepsy type one, is a neurodegenerative disorder characterized by action and stimulus sensitive myoclonus, tonic clonic seizures, progressive cerebellar ataxia, preserved cognition and poor outcome. The authors report clinical, neurophysiological, radiological and genetic findings of anEmirati family with five affected siblings and review literature. Methods All data concerning familial and clinical history, neurologic examination, laboratory tests, electroencephalogram, brain imaging, and DNA analysis were examined. Results Genetic testing confirmed the diagnosis of autosomal recessive progressive myoclonic epilepsy type 1 (EPM1) in two males and three females. Median age of onset was three years. Action or stimulus sensitive myoclonus and generalized seizures were recorded in 100%, at median age of onset of 3 and 4 years respectively. Multi segmental myoclonus and generalized status myoclonicusobserved in 80%. Dysarthria and ataxia developed in 100%. Vitamin D deficiency and recurrent viral infections noticed in100%. Cognitive, learning and motor dysfunctions involved100%. Sphincters were affected in 60%. Abnormal EEG recorded in 100%. Generalized brain atrophy accumulated in 60%. Phenytoin and carbamazepine used in 60% with worsening effect. Valproate and leviteracetam used in 100% with improving effect. Conclusions This is the first reported family of EPM1 in UAE. Our study emphasized a particular phenotype expressed as earlier disease onset, severe myoclonus,and generalized seizures. Cognitive, cerebellar, motor, and autonomic dysfunctions and brain atrophy were also earlier in onset and more severe than previously reported. Recurrent viral infections are another unique feature. This constellation in tout à fait was not previously reported in the literature.

Biography:

Abstract:

Purpose Progressive myoclonic epilepsy type one, is a neurodegenerative disorder characterized by action and stimulus sensitive myoclonus, tonic clonic seizures, progressive cerebellar ataxia, preserved cognition and poor outcome. The authors report clinical, neurophysiological, radiological and genetic findings of anEmirati family with five affected siblings and review literature. Methods All data concerning familial and clinical history, neurologic examination, laboratory tests, electroencephalogram, brain imaging, and DNA analysis were examined. Results Genetic testing confirmed the diagnosis of autosomal recessive progressive myoclonic epilepsy type 1 (EPM1) in two males and three females. Median age of onset was three years. Action or stimulus sensitive myoclonus and generalized seizures were recorded in 100%, at median age of onset of 3 and 4 years respectively. Multi segmental myoclonus and generalized status myoclonicusobserved in 80%. Dysarthria and ataxia developed in 100%. Vitamin D deficiency and recurrent viral infections noticed in100%. Cognitive, learning and motor dysfunctions involved100%. Sphincters were affected in 60%. Abnormal EEG recorded in 100%. Generalized brain atrophy accumulated in 60%. Phenytoin and carbamazepine used in 60% with worsening effect. Valproate and leviteracetam used in 100% with improving effect. Conclusions This is the first reported family of EPM1 in UAE. Our study emphasized a particular phenotype expressed as earlier disease onset, severe myoclonus,and generalized seizures. Cognitive, cerebellar, motor, and autonomic dysfunctions and brain atrophy were also earlier in onset and more severe than previously reported. Recurrent viral infections are another unique feature. This constellation in tout à fait was not previously reported in the literature.

Biography:

Dr. Pant received his M.A. and Ph.D. degrees in Physics from Agra University, Agra, India. His postdoctoral studies were conducted on the mechanisms of electron and ion transport in model membrane systems at the Department of Biophysics at Michigan State University. He joined the Laboratory of Neurobiology in the NIMH as a senior staff fellow in 1974 with Dr. Ichiji Tasaki where he studied the function of the axonal cytoskeleton in the squid giant axon. In 1979 he moved to the NIAAA extending his studies on the neuronal cytoskeleton and the effects of alcohol on its regulation. Dr. Pant moved to the NINDS, Laboratory of Neurochemistry in 1987 where he is presently chief of the section on Cytoskeleton Regulation. His laboratory is studying the mechanisms of topographic regulation of neuronal cytoskeleton proteins by post-translational modification, including the role of kinase cascades in normal brain and during neurodegeneration

Abstract:

Besides the hallmark pathology of amyloid plaques and neurofibrillary tangles (NFTs), it has been well documented that cyclin-dependent kinase 5 (Cdk5), a critical neuronal kinase in nervous system development, function and survival, when deregulated and hyperactivated induces AD and ALS like phenotypes in mice. Under physiological conditions, Cdk5 activity is tightly regulated. The deregulation and hyperactivation of Cdk5/p25 induces neuropathology. Thus Cdk5/p25 becomes prime therapeutic target for AD and neurodegenerative diseases associated with the hyperactivation of Cdk5. In order to prevent hyperactivation of Cdk5/p25, we have designed several small peptides of p25 on the basis of Cdk5/p25 crystal structure and checked for competition with p25 and thus inhibiting selectively the hyperactivity of Cdk5. We discovered a small peptide (p5) comprising of 24 amino acids, inhibited Cdk5 hyperactivation. The modification of p5 to TFP5 crosses BBB, was tested in a transgenic AD and ALS model mice. The p25 transgenic AD model (p25Tg) and 5XFAD mice were chosen since these mice show similar phenotypes to AD patients. Post TFP5 injections in p25Tg mice, 5XFAD and ALS model mice displayed significant reduction in Cdk5/p25 hyperactivity, A- beta plaque formation along with AD behavioral rescue. TFP5 does not inhibit normal Cdk5/p35 activity, and therefore has no toxic side effects. In addition, treated mice rescued synaptic dysfunction, neuroinflammation and a reduction in phospho-neurofilaments / tau and cell death. These results indicate that TFP5 has a potential to be a therapeutic target for AD.

Biography:

Gülsel YurtdaÅŸ KırımlıoÄŸlu got her Msc on “Inclusion complexes with antifungal agents” in 2010. She had completed her PhD study “Nanosized drug delivery system interfering epileptic mechanism” in 2014. Since 2008 she has been working as a Research Assistant at the Department of Pharmaceutical Technology at Anadolu University. Her researches focuses on novel technologies to enhance drug delivery.

Abstract:

Gamma aminobutyric acid (GABA), serves as the major inhibitory neurotransmitter, has a central role in neural control. Inhibition of GABA synthesis, blockage of release or postsynaptic reaction were determined to provoke convulsions. Significant reductions in brain GABA concentration were seen in patients with different epileptic syndromes. Several new approaches are being developed in an attempt to increase the entry and persistence of antiepileptic agents in the brain. One of the main strategy is nanosized drug delivery systems for the treatment of epilepsy. Halloysite nanotubes (HNT) is natural aluminosilicate clay with hollow tubular structure which allows loading drugs inside nanotubes lumens. In this study, GABA was successfully incorporated into HNT depending on the most recent epilepsy theory related to GABA. Characterization, drug loading, in vitro release studies and cytotoxicity test were performed on HNTs. Anticonvulsant effect of drug loaded HNT system were evaluated using pentylenetetrazole induced epileptic rats for in vivo studies. The latency to myoclonic jerks and incidence of generalized tonic clonic seizures with loss of righting reflex were noted as seizure parameters.

Biography:

Dr. Dana Byrd completed his PhD at the age of 29 years from University of Florida and postdoctoral studies from Columbia University School of Medicine.She has published more than 15 papers in reputed journals.

Abstract:

A biomarker in newborns at risk of developing Autism would be obviously highly valuable, allowing for very early intervention. Cerebellar structural and functional abnormalities have been found in individuals with Autism, as have been found abnormalities in the cerebellar-cortical-mediated learning, conditioning of eye blink. In the first two studies presented, we show behavioral and electroencephalographic evidence that sleeping newborn infants can present eye blink conditioning to a tone. In a third study, we produce evidence that 1-month-old infants’ eye blink conditioning is more rapid when the conditioned stimulus is a human voice as compared to a tone. These research studies have only been conducted on healthy infants, who are at no additional risk for Autism. However, research with populations at risk for Autism may show that these paradigms and their behavioral and electroencephalographic measures of conditioning may be able to detect atypical cerebellar functioning in at-risk populations. It should be pointed out that while these behavioral and electroencephalographic measures of conditioning to tones show some promise for determining risk for Autism, they are not as a diagnostic tool, but instead are a biomarker for risk for general cerebellar-cortical dysfunction, which is not only present in Autism but in other disorders as well such as Attention Deficit/Hyperactivity Disorder and Dyslexia. There is stronger hope for a specific biomarker for Autism in the form of atypical conditioning to the human voice since individuals with Autism have been found to process spoken stimuli differently than individuals without Autism.

Biography:

Alessandro Morelli (b. 1943) has studied enzyme Glucose-6-P-dehydrogenase and it’s molecular mechanism of senescence. Has been working in the field of phototransducion and molecular events in photoreceptor cells of vertebrate retina. He has discovered the protein FX, a NADP dependent enzyme catalizing synthesis of GDP-L-fucose. He has been working on the effects of electromagnetic fields of extremely low frequency on the activity of enzymes involved in bioenergeticprocess. Recently he has studied the myelin energetic function in brain put in in evidence the ATP extramitochondrial synthesis, with application in the study of Multiple Sclerosis and other neurodegenerative deseases.

Abstract:

In the last years, we have focused our attention on the role of myelin sheath as an energy supporter for the nervous conduction [1]. We have observed that myelin is able to conduct and extramitochondrial oxidative phosphorylation, consuming oxygen to produce ATP [2]. Moreover, we have also demonstrated a direct connection among myelin sheath and neuron, which may allow the transfer of ATP from the sheath to the axon [3]. Interestingly, the energetic role of myelin sheath was recently confirmed by Gat-Viks et al, studying the alteration of the energetic metabolism in the vanish white matter disease [4]. This finding introduces two new paradigms, one in bioenergetic and the other in neurobiology. Firstly, our data demonstrated that mitochondria is not the only “power-house”, but the OXPHOS proteins could be exported to other membranous structure, to provide a more efficient energy production [5]. Moreover, our hypothesis on the energetic function of myelin sheath sheds a new light on the role of this structure, giving a possible explanation of the neuron degeneration observed in the demyelinating diseases, as Multiple Sclerosis

Biography:

Dr Laurence Lacoste has completed his PhD at the age of 32 years from Nanterre University in France and postdoctoral studies from INSERM. She has worked in reputed Hospital in Paris as psychologist and as teacher in reputed French University. Now, she works asliberal psychologist and for the ethical research committee of Saint Louis Hospital in Paris. She has published more than 10 papers in reputed journals of medicine and psychology.

Abstract:

Lots of consultations exist at the moment to evaluate cognitive capacities of the Elderly. When elderly people begin to have memory problems, they often want to know if something is possible to help them and to have the opinion of specialists. Sometimes, it’s a member of the family, a general practitioneror a doctor of a hospital who do this request when they think that an elderly people begin to have troubles of memory or behavior. Also, when an elderly people is in an institution, neuropsychological evaluations are often asked. In geriatrics institutions, where there are people with Alzheimer disease or related disorders, neuropsychological evaluations are most often also present. In some epidemiological studies, neuropsychological evaluations are done from several years to try to find factors of risks and protection from pathological ageing. In this talk, we describe the interests of a neuropsychological evaluation, how we can do it with anamnesis and neuropsychological tests in the way to take care of the patientsand to answer to initial request. We also try to give the limits of this evaluation according to the question which is to treat and according to the way of the return which is done. It depends of each case, and it is not the same for the patient, the family the general practitioner, the other doctors in hospital, the members of an institution where is the patient for the end of his life or the public health.Finally, we try to give a general view of criticism and interest of early cognitive evaluation for the Elderly.

Biography:

His Current Position: Lecturer assistant at Department of Chemistry, Faculty of science, University of Cairo, Egypt. He is a Postdoctoral researcher at Institute of Physics, Rostock University, Germany . Education: Bachelor of Science in Chemistry (May 2005), Faculty of Science, University of Cairo “Excellent with Honor”. He did his Pre-Master in Physical Chemistry (October 2006), University of Cairo. Master of Science in Physical Chemistry (August 2009), University of Cairo, thesis entitled “Theoretical investigation of H-bond structure and dynamics in molecules of biological interest”. He did Ph.D. in Physical Chemistry (November 2013), University of Rostock, thesis entitled ’’Binding of chlorinated environmentally active chemicals to soil surfaces: chromatographic measurements and Molecular dynamic simulations’’.

Abstract:

Complications of diabetes mellitus include cognitive impairments and functional changes in the brain. The present study aimed to investigate the possible beneficial effect of vitamin D3 on episodic memory and cholinergic transmission in the prefrontal cortex of streptozotocin-induced diabetic rats. Methods: 30 male Wistar rats (150-200 gm) were included into control, diabetic and diabetic supplemented with vitamin D3 groups. Diabetes was induced by single intraperitoneal injection of streptozotocin (stz) 45mg/kg in citrate buffer. Vitamin D3 was administered orally in a dose of 500 IU/kg/day in corn oil for 10 weeks. Then rats were subjected to novel object recognition test to examine for episodic memory. Animals were sacrificed under diethyl ether anesthesia and prefrontal cortices were dissected to measure the activity of choline acetyl transferase (CAT) and acetyle choline esterase (ACE) enzymes to assess for cholinergic transmission. Results: Diabetic rats spent significantly less time exploring the novel object compared to control animals. Vitamin D3 significantly attenuated the diabetes-induced impairment so that animals again spent significantly more time exploring the novel object. The CAT activity was significantly decreased in diabetic animals while the ACE activity was significantly increased compared to control non-diabetic animals. Diabetes-induced alterations in enzyme activity in the prefrontal cortex were mitigated by vitamin D3 supplementation. Conclusion: The present findings demonstrate the potential effect of vitamin D3 supplementation on cognitive function in diabetic animals. It is possible that this effect was mediated through enhancing the prefrontal cortex cholinergic transmission.

Biography:

M.B.B.S ,1991. School Of Medicine, University Of Salah AL-deen, Erbil - Iraq Jordanian Board of Pediatrics, Jordanian Medical Council, Sep 1999 , Clinical Fellow (SpR Level) in Pediatric neurology at King Hussein Medical Center Amman-Jordan / Royal Medical Services(RMS) from January 2003. Post doctorial clinical trainee in Pittsburgh children hospital- Neurological Department 2005-2006, Head of Pediatric Neurology and neurophysiology atQueen Rania Hospital for Children Royal Medical Services

Abstract:

Objective: The present study was done in order to obtain a baseline profile of infantile spasms and associated neurological disorders. Patient and methods:. The study included 50 patients with infantile spasm in Queen Rania Hospital for children in Jordan. The following data were obtained: sex, age at onset of spasms, details of seizure, family history of epilepsy, significant pre-/peri/post-natal insults, Electroencephalography and detailed neuroimaging evaluation , detailed neurological, neuro developmental ,assessment were done by. Broad categories of possible etiologies were used the results were recorded for further study. Results: Age of onset of infantile spasms ranged from 1month to 1 year and 6 months , (mean 4.8 months). The mean time of presentation was 9.4 months . A male preponderance was noted (74 %). flexor spasms (52%) was the commonest . Other types of seizures also accompanied infantile spasm in 44% children . (84%) were born of normal delivery, History of birth asphyxia was obtained in 48%, 3 (6%) had positive family history Developmental delay was recognized prior to onset of spasms in 52%, microcephaly was the commonest associated problem, Imaging studies of the brain revealed abnormality in 18 patients. 78% patients were classified as symptomatic and 22 % as cryptogenic. Conclusion and recommendation: the pattern of infantile spasm in our country do not differ from that of developed countries, further researches is required to prevent both chronic epilepsy and psychomotor retardation and .preventive measurement to prevent birth asphyxia is recommended

Biography:

Jirapast Sichaem has completed his PhD at the age of 26 years from Chulalongkorn University. He is doing postdoctoral studies in the field of anticholinesterase compounds from Thai medicinal plants at Natural Products Research Unit, Department of Chemistry, Faculty of Science, Chulalongkorn University. He has published more than 22 papers in scientific journals.

Abstract:

Alzheimer's disease (AD) is the most common cause of neurodegenerative disorder and dementia in elderly people. The cholinergic hypothesis proposes that AD is caused by reduced synthesis of the neurotransmitter acetylcholine (ACh) in the brain. In addition, a substrate non-specific butyrylcholinesterase (BChE) is also found to play a significant role in the hydrolysis of ACh. Moreover, there are several reports that have revealed that the reduction of AChE activity can be compensated for BChE activity. Thus, all of the above reasons have stimulated a great interest in screening natural cholinesterase (ChE) inhibitors as lead compounds for the intended treatment of AD as they should have significant inhibition activities towards both AChE and BChE. Previous reports have shown that some furoquinoline alkaloids and other constituents of the plants from Rutaceae family have ChEs activities revealed to the treatment of AD. Therefore, the successive extraction and isolation of bioactive ChE inhibiting compounds from the plants of this family were interesting, as they can themselves be active and used directly as a drug. Evodia lepta (Spreng.) Merr. (Rutaceae) is a traditional medicinal plant used for the treatment of arthritis, fever, chickenpox, epidemic influenza, meningitis, infectious hepatitis, antipruritic, depurative and febrifuge diseases. Several furoquinoline alkaloids, flavonoids and chromones have been also reported from this plant in previous studies. Three new furoquinoline alkaloids (1-3) along with six known furoquinoline compounds (4-9) were isolated from the leaves of Evodia lepta based on bioassay-guided fractionation and chromatographic techniques. All isolates were evaluated for their in vitro cholinesterase (ChEs) inhibitory activities, in which compounds 7 and 5 exhibited the highest activity toward AChE and BChE, respectively. Lineweaver-Burk plots indicated that 5 and 7 were mixed mode inhibitors of both ChE enzymes. Finally, the molecular docking studies on the binding sites of AChE and BChE were performed in order to afford a molecular insight into the mode of action of these active compounds in a good agreement with their anti-ChE results. Therefore, this information can help in designing a new inhibitor in the class of furoquinoline alkaloids in against Alzheimer’s disease.

Biography:

Alessandro Morelli (b. 1943) has studied enzyme Glucose-6-P-dehydrogenase and it’s molecular mechanism of senescence. Has been working in the field of phototransducion and molecular events in photoreceptor cells of vertebrate retina. He has discovered the protein FX, a NADP dependent enzyme catalizing synthesis of GDP-L-fucose. He has been working on the effects of electromagnetic fields of extremely low frequency on the activity of enzymes involved in bioenergeticprocess. Recently he has studied the myelin energetic function in brain put in in evidence the ATP extramitochondrial synthesis, with application in the study of Multiple Sclerosis and other neurodegenerative deseases.

Abstract:

In the last years, we have focused our attention on the role of myelin sheath as an energy supporter for the nervous conduction [1]. We have observed that myelin is able to conduct and extramitochondrial oxidative phosphorylation, consuming oxygen to produce ATP [2]. Moreover, we have also demonstrated a direct connection among myelin sheath and neuron, which may allow the transfer of ATP from the sheath to the axon [3]. Interestingly, the energetic role of myelin sheath was recently confirmed by Gat-Viks et al, studying the alteration of the energetic metabolism in the vanish white matter disease [4]. In the last years, we have focused our attention on the role of myelin sheath as an energy supporter for the nervous conduction. We have observed that myelin is able to conduct and extramitochondrial oxidative phosphorylation, consuming oxygen to produce ATP. Moreover, we have also demonstrated a direct connection among myelin sheath and neuron, which may allow the transfer of ATP from the sheath to the axon. Interestingly, the energetic role of myelin sheath was recently confirmed by Gat-Viks et al, studying the alteration of the energetic metabolism in the vanish white matter disease. This finding introduces two new paradigms, one in bioenergetic and the other in neurobiology. Firstly, our data demonstrated that mitochondria is not the only “power-house”, but the OXPHOS proteins could be exported to other membranous structure, to provide a more efficient energy production. Moreover, our hypothesis on the energetic function of myelin sheath sheds a new light on the role of this structure, giving a possible explanation of the neuron degeneration observed in the demyelinating diseases, as Multiple Sclerosis.

Biography:

Dr. Hamed A. Benghuzzi, professor of health sciences at UMC, has been elected as the president of the Mississippi Academy of Sciences.Benghuzzi earned his PhD at the University of Dayton.He completed a pathology fellowship at the University of Michigan.He joined the UMC faculty in 1993 as assistant professor of health sciences.

Abstract:

Manipulation of gonadotropin hormones (luteinizing (LH) and follicle stimulating hormones (FSH)) in ewes in non-breading season is a major challenge to the scientific community. We hypothesized that sustained delivery of progesterone and estrogens by means of Tricalcium-Phosphate-Lysine delivery systems (TCPL) can suppress the rise in LH and FSH levels and ultimately induce cycling activities. The specific objective of this study was to design an implantable TCPL system capable of delivering progesterone (P) for about two weeks and Estradiol (E) in a short burst that mimics the ovulatory surge in adult ewes. TCPL implants were fabricated in four different sizes (1.5, 2.3, 3.5, or 5.6 cm) using four different ceramic compositions and impregnated with P (20-45%) and E (4-16%). Surgical aseptic techniques were employed following standard approved lab protocols. Blood samples were collected daily and anlyzied for P, E, LH and FSH levels. X-ray procedure was performed twice a week to assure the intactness of the devices. The results of this student revealed: (1) TCPL were cable of delivering P and E at levels that mimic the estrus cycle, (2) remarkable reduction of LH and FSH levels in all experimental animals compared to sham operated group. Overall conclusion, results of this study demonstrated that the anterior pituitary gonadotropin hormones can be regulated through sustained delivery of reproductive hormones.

Biography:

Tarit Kanti Ghosh MSc, MBBS, born in 1968 is a renowned Neurologist in Bangladesh. Since the very childhood he was extraordinary talented i.e. he always stood as topper in the class. In secondary school certificate & higher secondary certificate public exam he was one of seven among about 400,000 students all over the country. Being a son of a doctor his ambition was to become a benevolent physician. Thereby, he completed his graduation from the then British recognized medical college in Dhaka, Bangladesh in 1993. Then he did post-graduation(MSc) in internal medicine & Neurology from United Kingdom. He accomplished “Leading edge neurology for the practising clinicians, 2014” course in University college of London, UK. Due to thirst of knowledge he is still studying in the university of Melbourne, Australia in the Specialist Certificate Course in Clinical Research Neuroscience.

Abstract:

In this article I shall be trying to show how surgery irrespective to age and/ or organ becomes a prospective major health problem. In general about 50-60% patients undergone anyhow surgery suffer mild/moderate/severe psychobiological illness in future for a long time due to feeling of fear that he/she (1:3)(1) has lost part of his body, inside unhealed or prolonged healing process . So anxiety, tension, emotion and depression gradually burden their daily life style eventually leading to chronic stress (about 10%) in 4 years after surgery along with some major health risk. Background: This is an observational, prospective and multi centred study under intention to treat principle. This study is a over-view about the patients from January’08 to July’14. Data was collected from the leading practitioners of a district named Khulna in Bangladesh. The practitioners are Medicinist, Gynaecologist, Orthopaedician, Eye Surgeon, General Surgeon, Psychiatrist and Neurologist. In this study the outcome shows that about 10% of post surgical (mainly those who were undergone major surgery) had been suffering from chronic stress and among them some patients experienced major health risks i.e. Hypertension, Diabetes, Stroke, Heart attack, Panic disorder, Generalised Anxiety Disorder etc.

Biography:

Fakhir Al-Ani has completed his M.Sc. study and PhD study from Baghdad University ,College of Medicine. School of Medicine. He spend about 30 yars as a teaching staff in medical college. He is now working in Mutah University, Medicl College as the head of Physiology & Pathology Dept. He has supervised more than 13 Ph.D thesis, and more than 23 M.Sc. thesis. He has published more than 35 papers in reputed journals.

Abstract:

The bizarre confusing symptoms of multiple sclerosis (MS) with its remission and relapse property, and the unavailability of a single neurological or laboratory test, which can definitively confirms or rules out MS, make it difficult to be diagnosed. Cerebrospinal fluid (CSF) analysis is often performed in cases of suspected MS to identify the elevation of immunoglobulin (mainly IgG) in the form of oligoclonal band. Although CSF as a test is a highly useful test in the diagnosis of MS, but it is not free of risk and complication moreover it can not be performed frequently. It had been noticed that the tears of MS patients compose immunological abnormalities, namely, increased immunoglobulin levels (mostly IgG), and the appearance of oligoclonal bands in electrophoresis like that of the CSF analysis. Accordingly in this study we tried to explore the significant of tear analysis in the diagnosis of MS. Materials and methods: Fifty six tear samples were tested; those include normal subjects, MS patients, and patients with other neurological diseases Collection of tears after simple induction of lacrymation., the microns of this tears were used. Tear electrophoresis using conventional SDS polyacrylamide gel electrophoresis according to the recommendations of LKB was used. Results Tear electrophoresis had showed two specific bands appearing in tear samples of multiple sclerosis patients, which were absent in samples of normal subjects. One band appeared in the immunoglobulin region. While the second band had a lower molecular weight, which was about 25 kD. It had been noticed that the tears of MS patients compose immunological abnormalities, namely, increased immunoglobulin levels (mostly IgG), and the appearance of oligoclonal bands in electrophoresis like that of the CSF analysis. Accordingly in this study we tried to explore the significant of tear analysis in the diagnosis of MS.

Biography:

Dr. Hiroshi Nakanishi is currently a Professor of Department of Aging Science and Pharmacology, Kyushu University. He completed his PhD in Kyushu University and his post-doctoral trainingin the University of Tennessee at Memphis. He became a Professor of Laboratory of Oral Aging Science, Kyushu University in 2000. He was the Dean of Faculty of Dental Science, Kyushu University from 2011 to 2013. He is now the vice Dean Faculty of Dental Science, Kyushu University from 2014. His research is focusing on the physiological and pathological functions of microglia in the central nervous system.

Abstract:

A group of proteases in the endosomal/lysosomalproteolytic system have been designated as cathepsins, which is derived from the Greek term meaning “to digest”. Considering that cathepsins can irreversibly cleave peptide bonds, the primary function of cathepsins has been believed to be their “disintegration actions”. However, there is increasing evidence that cathepsins can also exert “modulator actions” by which substrates are activated after limited cleavage. For examples, we have recently found that cathepsin B (CatB) is involved in the maturation of pro-IL-1through proteolytic activation of pro-caspase-1 in the autophagosomes of spinal microglia following peripheral inflammation, leading to the induction and maintenance of inflammatory pain.On the other hand, cathepsin S (CatS) is involved in proteolytic processing of the MHC class II-associated invariant chain in splenicdendritic cells following peripheral nerve injury, leading to activation of CD4+ T cells. Infiltration of activated CD4+ T cells may contribute to transition of nerve injury-induced acute pain to a chronic pain state.Beyond a bulk proteolysis in the endosomal/lysosomal system, the growing understanding of modulator actions of cathepsins in microglia and other mononuclear phagocytes could contribute to the development of protease inhibitors as therapeutic interventions against brain diseases associated with chronic inflammation and immune response.

Biography:

Benjamin Chitambira completed his BSc Physiotherapy Honours degree from the University of Zimbabwe in 1995. He also completed a Postgraduate Certificate in Healthcare Leadership from the Open University in the UK in 2014. With over 19 years’ experience as a neuro-physiotherapist, he has been carrying out research on optokinetic chart stimulation as a clinical specialist physiotherapist in the Richard Stevens Stroke Unit for over 8 tears.With over 9 papers published in peer reviewed journals, he has been a peer reviewer for reputable journals and now serves as an editorial board member of peer reviewed journals.

Abstract:

Background: This presentation aims to describe optokinetic chart stimulation and its evolution as a recovery focused neurorehabilitation intervention. Stroke, traumatic brain injuries and critical care polyneuropathy and or myopathy can cause severe disability.
Methods: The optokinetic chart is made of laminated A4 paper. It consists of repeated bundles of the colours of the rainbow. The chart is placed 20 centimetres in front of a patient’s face. It is moved from side to side atapproximately one cycle per second for 3 minutes. This is followed bymoving the chart up and down for 3 minutes and then forwards and backwards for another 3 minutes.
Results: The first task was to identify which strokes benefited most from the intervention. A case seriespublished in 2011 identified that strokes not involving simultaneous infarcts or haemorrhages of parietal and temporal lobes recovered movements. A case control series published in 2014 demonstrated statistically significant upper limb recovery (P<0.05). The author has been pilot-testing to see if these differences are reproducible under randomized controlled trial conditions. First set of comparable results point to the potential of a future full trial achieving an all and none principle of the ideal scientific experiment. Preliminary efficacy has also been demonstrated in difficult to rehabilitate traumatic brain injuries and critical care polyneuropathies and or myopathies.
Conclusion: Optokinetic chart stimulation shows promise as a novel recovery focused neurorehabilitation intervention. Further research with fully powered studies is required to provide evidence for its inclusion in future guidelines.

Biography:

Fakhir Al-Ani has completed his M.Sc. study and PhD study from Baghdad University ,College of Medicine. School of Medicine. He spend about 30 yars as a teaching staff in medical college. He is now working in Mutah University, Medicl College as the head of Physiology & Pathology Dept. He has supervised more than 13 Ph.D thesis, and more than 23 M.Sc. thesis. He has published more than 35 papers in reputed journals.

Abstract:

Fibrin sealant “fibrin glue" is a unique surgical hemostatic/adhesive material. It is a natural, biocompatible and biodegradable material, resembling the final step of the coagulation cascade. It is composed of cryoprecipitate, thrombin and anti-fibrinolytic agent. Fibrin sealant is being utilized with increasing frequency in a variety of surgical situations with a wide range of clinical applications for suture support, tissue adhesion, and hemostasis. In clinical use, many factors may influence the outcome like; the time of clotting onset, the duration before lysis, biocompatibility, as well as some of its biomechanical properties such as tensile strength and elasticity. The aim of this study was to assess the optimization of the biomechanical criteria which are important for the surgeons for each specific surgical task. The method that we use is to synthesis fibrin glue with different concentrations and additions (tranexamic acid, platelets). Then we monitor the clotting times, durations need for clot to lysis, as well as explore the biomechanical behavior (tensile strength and elasticity). Synthesis of the glue revealed significant increase clotting times and durations for clot lysis when cryoprecipitate concentration was increased and when tranexamic acid or platelets are added to the glue. The elasticity tests clarified that the increase of cryoprecipitate concentration or tranexamic acid addition to fibrin glue formula caused significant higher elasticity. On the other hand, platelets or both tranexamic acid and platelets additions caused significant decrease elasticity results, which increase with time. The tension tests revealed that the increase of cryoprecipitate concentration or additions of platelets or both tranexamic acid and platelets caused significant higher resistance to tension, and this resistance decreases with time, while the addition of tranexamic acid alone causes a significant decrease in tension results, which increase with time. The biocompatibility was studied for all the components by a rat models with severed sciatic nerve was employed to evaluate the clinical efficacy of the glue. The results present gradual clinical improvement of the paralyzed leg with symmetrical bilateral movements at 6 weeks to 2 months duration. In conclusion, changing the concentration of the cryoprecipitate in relation to the thrombin and the addition of tranexamic acid and or platelet can change the duration, elasticity and tensile strength to make it compatible for specific operation.

Biography:

Dr Nick Cunniffe graduated from Cambridge University with degrees in neuroscience and medicine. After completing junior years in Cambridge, he is now undertaking specialist training in London, while lecturing neuroscience at the University of Cambridge and continuing to conduct research with Prof. Carpenter who was originally invited to this meeting, but prevented from travelling by a medical condition: Dr Cunniffe is representing him. Roger Carpenter is Emeritus Professor of Oculomotor Physiology at Cambridge, and directed medical studies for many years at Gonville and Caius College. Well known as the author of the classic Movements of the Eyes, he has published many papers using eye movements to study decision mechanisms of the brain (the LATER model) and their clinical applications. He is also the author of the highly successful Neurophysiology, now in its fifth edition.

Abstract:

The study of saccadic latency, the variable time between presentation of a peripheral stimulus and foveation of the target, has provided important insights into the neural mechanisms underlying reaction times and decision. It has emerged as a powerful tool to quantify neurological impairment in a wide range of conditions. Patients with Huntington’s disease and Frontotemporaldementia, for example, generate saccades with significantly increased latency. In Parkinson’s disease meanwhile, saccadometrydemonstrates how neural function is affected by the disease and its treatment, for example deep brain stimulation. Our latest work has shown measurement of saccadic latency distributions in patients with liver cirrhosis can accurately detect Covert Hepatic Encephalopathy (CHE). This cognitive defect, found in 30-70% of cirrhosis patients, has been linked to poor quality of lifeand increased mortality, while early detection and appropriate treatment may reverse the deficit. Despite its clinical significance, diagnosis relies on psychometric tests that have proved unsuitable for clinical use. Our study diagnosed CHE in a subset among 36 cirrhosis patients by subjecting them to the World Congress of Gastroenterology standard of psychometric tests. We then used a portable saccadometer to measure their saccadic eye movements. We found those with CHE (16) had significantly prolonged saccadic latencies when compared with those without (20). There was in fact a spectrum of cognitive impairment among cirrhosis patients, with those defined as having CHE by psychometric testing having slower reaction times. Saccadometry therefore represents an opportunity for accurate and early diagnosis of CHE, better informing treatment in these patients.

Biography:

Preshita Desai is an INSPIRE-Fellow currently pursuing Ph.D. (Tech.) in Pharmaceutics at Institute of Chemical Technology, India under Prof. Vandana Patravale. She has two patents, two reviews, two scientific publications in peer-reviewed international journals and a book chapter to her credit. She has presented 13 scientific abstracts in national and international proceedings and has received awards for 11. She was recently bestowed with Ranbaxy Science Scholar Award 2014. Her research interests include synthesis and application of novel lipid bioconjugates for targeted delivery to central nervous system, exploring hot melt extrusion, high pressure homogenization techniques toward bioenhancement of poorly bioavailable drugs.

Abstract:

Curcumin -a polyphenol, exhibits strong anti-oxidant, neuroprotective and anti-amyloid potential that makes it a potent candidate for alleviation of oxidative stress induced neurodegenerative ailments viz. Alzheimer’s disease. Though potent, its clinical translation is restricted due to poor aqueous solubility (~11ng/ml in pH5 aqueous buffer), chemical instability and meager permeability across brain barrier. This demands a smart nanodelivery platform that will not only ensure the drug stability but will also facilitate drug transport across brain barrier. With this rationale, we propose curcumin loaded targeted micellar nanocarriers (t-micelles) comprising a novel lipid bioconjugate (t-bioconjugate) with an ability to cross brain barrier via receptor mediated active transport. The synthesized t-bioconjugate was characterized for its physicochemical properties, safety and brain permeation efficacy both in vitro and in vivo. The curcumin loaded t-micelles exhibited a spherical geometry (size:21.3±2.68 nm, PDI:0.148) and demonstrated safety and acceptable properties for nasal spray application. In vitro anti-oxidant assay revealed 1.6 fold better anti-oxidant activity (DPPH assay) of curcumin loaded t-micelles in contrast to curcumin loaded plain micelles and could be attributed to mild antioxidant potential of t-bioconjugate. In vivo pharmacokinetic and biodistribution studies demonstrated enhanced brain transport of t-micelles via active transport and curcumin was quantified in brain tissue upto 12 hours predominantly in the olfactory region, hippocampus and cerebellum of the brain. The developed formulation was stable as per ICH stability guidelines. The studies corroborated the potential of t-micelles as a platform and potential strategy in treatment of neural ailments to enhance brain bioavailability of therapeutic actives.