Thomas Eko Purwata is a Senior Lecturer at one of the most renowned public-funded university hospital in Indonesia. He was a well-experienced Consultant Neurologist in the fi eld of pain and peripheral nerve. In addition, he has conducted an extensive research in the corresponding area-of-expertise with numerous publications and proceedings. Currently he is also an active Member and Fellow of the American Association of Neurology.

To date, there has been limited evidence linking erectile dysfunction (ED) aft er stroke. Th e mechanism of ED aft er stroke has not yet been fully elucidated. In fact, there has been a limited insight regarding the underlying prognostic factor of ED aft er stroke incident. Several studies had attempted to link the site of stroke lesion along with its comorbid factors with ED. Accordingly this study was conducted in order to identify any positive relationship between left hemispheric lesion and ED among stroke subjects. Th is was a cross-sectional observational study design. All subjects who fulfi lled the inclusion-exclusion criteria were assigned into two groups, i.e. those with left or right hemispheric lesion before interviewed for ED using IIEF-5. A total of 74 subjects were included in this study. In left hemispheric lesion, as many as 25 subjects (33.8%) suff ered from ED, while the rest (10 subjects; 13.5%) did not. Among subjects with right hemispheric lesion, there were 13 (17.6%) who suff ered from ED and 26 (35.1%) who did not. Th erefore, this study showed that left hemispheric lesion was positively correlated with ED in stroke subjects (r=0.361; p=0.032). Our study has confi rmed previous fi ndings which link left hemispheric lesion post stroke with ED. Future studies should be further directed to utilize the site of brain lesion as a risk as well as prognostic factor for ED among stroke subjects.

Goang Won Cho has completed his PhD program from Hanyang University (Seoul, Korea) and Postdoctoral studies from National Institutes of Health (NIH, USA) and Duke University (USA). He is the Professor of Chosun University. He has published dozens of SCI papers.

Neuronal degeneration induced by chronic oxidative stress is one of several etiological causes of neurodegenerative diseases. In this study, we investigated the functional role of histone methyltransferase G9a in oxidative stress-induced degeneration in human SH-SY5Y neuroblastoma cells. Using the MTT assay and immunoblot analysis, the viabilities of H2O2- treated cells decreased signifi cantly; however, treatment with the G9a inhibitor BIX01294 partially attenuated this eff ect. The expression of neuronal specifi c genes also decreased in H2O2-treated cells but recovered with G9a inhibition. H2O2-treated cells showed high levels of H3K9me2 (histone H3 dimethylated at the lysine 9 residue), which is produced by G9a activation, and BIX01294 treatment lessened the over-activation of G9a. The expression of repressor element-1 (RE-1)-containing neuronal specifi c genes increased in response to BIX01294 treatment as confi rmed by a chromatin immunoprecipitation (ChIP) assay with H3K9me2 antibody. Th e diff erentiation rates of SH-SY5Y cells also recovered with the inhibition of G9a in H2O2-treated cells, which was seen by immunoblot analysis of neuronal specifi c proteins. Th ese results demonstrate that oxidative stress induces the over-activation of G9a, disturbs the expression of neuronal specifi c genes, and progressively mediates neuronal cell death. Moreover, a G9a inhibitor can lessen G9a over-action and prevent neuronal damage. G9a inhibition may therefore contribute to the prevention of oxidative stress-induced neurodegeneration.

X Jiang is doing her PhD study in Germany Center for Neurodegenerative Disease, DZNE. She fi nished her Bachelor’s degree in Applied Mathematics and Master’s degree in Psychology. She has published three papers in reputed journals (e.g. Human Brain Mapping).

Goal of this study was to investigate the structural and functional changes in the cerebellum in sporadic ataxia with adult onset (SAOA), and to test for potential associations between structural-functional alterations in the cerebellum and disease duration. 37 SAOA patients (62.38±9.53 years) and 49 healthy controls (HC) (65.08±6.85 years) underwent a structural and resting state functional MR (rsfMRI) scan. Focusing on the cerebellum, we performed voxel-based-morphometry and a network analysis based on rsfMRI using degree centrality (DC) as key marker for network integrity. In order to investigate the role of the disease duration, we further divided the SAOA group into one group with long disease duration (n=15, duration = 13.27±3.75 years) and one with short duration (n=14, duration = 2.91±1.72 years). Group diff erences were calculated using twosample t-tests, controlling for age, gender and total intracranial volume (only structure) (p<0.01; FWE corrected, cluster-extent 20 voxels). Grey matter atrophy in SAOA was detected in bilateral cerebellar lobules I-V, V, VI, IX and X but no diff erences were found between SAOA long- and short-duration groups. Higher DC values were found in right cerebellar lobules VIII A/B and the dentate nucleus in SAOA patients when compared to HC. An increased DC was found in right cerebellar lobule V in SAOA patients with long as compared to short disease duration. Th e regions found are known to be involved in sensory-motor processing, being in line with clinical appearance of SAOA. Interestingly, the functional and structural findings do not overlap, potentially indicating that the structural alterations may cause the connectivity changes.

Sang Won Suh has completed his PhD in 2001 from University of Texas, Medical Branch, Galveston and Postdoctoral studies from University of California, San Francisco, School of Medicine. He is a Professor and an Associate Dean of Hallym University, College of Medicine. He has published more than 90 papers in reputed journals and has been serving as an Editorial Board Member of MDPI journal.

Acamprosate or N-acetyl homotaurine is a N-methyl-D-aspartate (NMDA) receptor antagonist that is used as a pharmacological means of treatment for chronic alcohol dependence. Although the exact mechanism of acamprosate has not been clearly established, it appears to work by promoting a balance between the excitatory and inhibitory neurotransmitters, glutamate and gamma-aminobutyric acid (GABA), respectively. Several studies have demonstrated that acamprosate provides neuroprotection against cerebral ischemia-induced brain injury. However, there are no studies investigating the role of acamprosate on traumatic brain injury (TBI) induced neuronal death. In the present study, we sought to analyze the therapeutic potential of acamprosate to protect against neuronal death and other underlying pathogenic mechanisms that arise following TBI. Rats were given acamprosate (200 mg/kg) orally once per day for two weeks. Two week later, rats were subjected to a controlled cortical impact (CCI; 5 m/sec, 500 ms duration, 5 mm deformation) injury over the right parietal cortex. Histological analysis was performed at 3 or 24 hours, or 7 days aft er TBI. We found that acamprosate treatment for 2 weeks reduces levels of vesicular glutamate and zinc in the hippocampus. Consequently, this reduced vesicular glutamate and zinc level resulted in reduction of ROS production at 3 hours aft er TBI. When evaluated at 24 hours aft er TBI, acamprosate administration reduced the number of degenerating neurons, blood-brain barrier (BBB) disruption, leukocyte infi ltration and dendritic loss. Acamprosate also reduced glial activation and neuronal loss at 7 days aft er TBI. In addition, acamprosate rescued TBI-induced cognitive dysfunction. Th e present study demonstrates that acamprosate attenuates TBI-induced brain damage by depletion of vesicular glutamate and zinc levels. Th erefore, the present study suggests that acamprosate may have a high therapeutic potential for prevention of TBI-induced neuronal death.

Tomas Budrys is a Radiologist working in the University Hospital at the Department of Radiology specializing in Nuclear Medicine and Neuroradiology. He is specialized in Nuclear Medicine and Neuroradiology. Tomas Budrys is a last year Doctoral student working as a Lecturer for more than three years, teaching students and residents. He has published three articles with Clarivate Analytics indexing. Currently, he is developing new radiology journal and maintaining many websites associated with radiology. Tomas Budrys research interests include medical physics, neuroradiology, nuclear medicine and safety in radiology. He is also a Member of the organizations like RSNA (Radiological Society of North America), ESR (European Society of Radiology) and LRA (Lithuanian Radiology Association).

Aim: Th e aim of the study is to compare the amount of epileptogenic foci found in EEG and PET/CT; determine most common localizations of epilepsy focal points in both functional and structural imaging methods; determine the success rate of surgery in the operated patients when the focal points of epilepsy coincided in all three imaging methods and; verify the concordance between the location of epileptogenic focal points found in EEG and PET/CT studies. Methods: We studied a group of 35 patients with clinically proven refractory epilepsy. All patients underwent an MRI, fl uorodeoxyglucose-18-PET scan, and an EEG. 14 patients underwent neurosurgical operation with removal of epileptogenic foci. Assessment of normality was verifi ed by the Kolmogorov-Smirnov and Shapiro-Wilk tests. Th e Wilcoxon signal criteria were used to compare the two dependent samples whose data did not match the normal distribution. Concordance was evaluated by using Cohen's kappa (κ). Results: PET/CT lesion quantity Sig. p<0.05/p<0.05; EEG epileptogenic foci quantity Sig. p<0.05/p<0.05. According to Wilcoxon signed ranks test we can make assertion that there is a statistically signifi cant diff erence between the number of epileptogenic foci found in PET/CT and EEG studies (Sig. 0.021<0.05). Most common localization for epileptogenic activity in all three methods was temporal lobe (39.6-48.6%). 10/14 patients who underwent surgery demonstrated excellent postsurgical outcomes, with no epileptic seizures; 3/14 patients had 1-2 seizures aft er surgery and 1/14 patient had same or more epileptic seizures. Measure of agreement kappa value was 0.637; asymptotic standardized errora was 0.096; approximate Tb was 6.253; approximate signifi cance was <0.005. Conclusion: Surgical treatment may off er high hope for patients with intractable epileptic seizures. PET/CT is extremely useful imaging method to assist in the localization of epileptogenic zones. The dynamic functional information that brain PET/ CT provide is highly complementary to anatomical imaging in MRI and functional information in EEG.

Ju Young Kim did her Bachelor’s degree in Pharmacy from Chungbuk National University and has worked at Chungbuk National University Hospital as a Pharmacist. After she worked as a local Pharmacist, she started her Master’s in the Clinical Pharmacy and she is working on clinical study using big data and interested in pharmacogenomics.

The association of type 2 diabetes mellitus (DM) and dementia has been investigated previously, but remains controversial. The aim of this observational study was to investigate the relationship between prior type 2 DM and dementia using a large population-based dataset. Data were collected from Korean’s National Health Insurance Research Database (2002- 2013), which released a cohort dataset of 558,147 randomly sampled elderly people and confirmed it to be representative of the Korean elderly population. We included 260,023 patients with type 2 DM as cases and 212,036 non-diabetes subjects without any diabetes diagnosis as control in this study. Demographic data such as age, gender, CCI (Charlson comorbidity index), comorbidities were compared with Student t test and chi-square tests. In addition, we performed a conditional logistic regression to examine the odds ratio (OR) and 95% confidence interval (CI) for dementia between cases and controls. During the observational period, 56,587 (21.7%) and 36,137 (17.0%) cases of dementia were detected in patients with type 2 DM and non-DM control group, respectively. Characteristics associated with dementia included hypertension (OR: 2.43; CI: 2.38, 2.48), stroke (OR: 4.48; CI: 4.41, 4.55), ischemic heart disease (OR: 1.78; CI: 1.75, 1.80) and hyperlipidemia (OR: 1.79; CI: 1.75, 1.80). Additional logistic regression analysis showed that the crude OR of dementia for cases was 1.35 (CI: 1.33-1.37) compared to controls. After adjusting for patients’ sex, age, CCI, comorbidities (hypertension, stroke, Ischemic heart disease, hyperlipidemia), the adjusted OR of dementia for patients with type 2 DM was 1.69 (95% CI: 1.66, 1.72) compared to those without DM.

Su Jin Noh has her expertise in drug development and evaluation in neurological disorders. She studied potential drug development by mechanism based targeting for curing neurodegenerative disease such as Alzheimer’s disease, Parkinson’s disease and stroke during her PhD program. Now she focuses on discovery of pathology of neuropsychiatric disease including schizophrenia or addiction.

We have recently demonstrated that DHED can reduce the generation of amyloid beta peptide by inhibiting beta-secretase (BACE-1) activity. In this study, carboxylated DHED (cx-DHED), soluble analogue of DHED was developed and its mechanism was investigated. Administration of cx-DHED (1 mg/kg) for four months resulted in more significantly lowering of brain amyloid beta peptide than that of DHED in Tg2576 mice. Moreover, cx-DHED ameliorates memory impairments and hippocampal cell death in Tg2576 mice. Treatment of 10 μM cx-DHED impedes amyloid beta peptide production in Tg2576 primary neuronal cell. Furthermore, cx-DHED significantly reduced beta-secretase activity and increased alphasecretase activity in an enzymatic activity test. 3D-QSAR study was shown that cx-DHED strongly binds substrate recognition domain of ADAM10 as well as BACE1. These results strongly suggest that cx-DHED may reduce the biosynthesis of amyloid beta peptide by inhibiting BACE1 and activating alpha-secretase concurrently. Combined with previous findings of direct inhibition of BACE-1 by DHED, this work indicates that carboxylating strategy on beta-secretase inhibitor may have potential to provide new insights into designing novel drugs that target multiple steps of aberrant amyloid precursor protein (APP) processing to treat Alzheimer's disease.

Azin Ebrahim Amini is a second year Master’s student at University of Toronto in the Department of Biomedical Engineering within Neuroscience platform. She has completed her Bachelor’s at University of Toronto where she double majored in Neuroscience and Physiology. She is interested in integrative sciences and that's why she continued her graduate studies in an engineering program after obtaining her Bachelor’s degree in Sciences. Her interest to multidisciplinary sciences motivated her to learn advanced programming software along with designing a new method for recording intracranial brain activities. Along with being active in academic world she also takes on community service responsibility and engages in leadership and mentorship programs.

Extracellular potassium ion concentration ([K]e) is tightly regulated throughout the brain because it has a major impact on brain functionality. Potassium concentration is disrupted in many brain diseases such as stroke and epilepsy. My project is designed based on a well-developed experimental platform to investigate the effects of extracellular potassium redistribution in physiological states. All experiments were conducted in vivo in mouse neocortex. Two double-barreled K-sensitive electrodes coupled with local field potential (LFP) electrodes were placed 4 mm apart. 50 mM KCl solution was injected focally closer to one of the K-LFP electrodes. [K]e levels and LFP were measured in two different scenarios: 1) Pharmacological intervention (gap junction blockage); 2) Optical intervention (optogenetics). Focally increased [K]e was associated with a transient depolarization which in turn spreads into neighboring tissues so called spreading depolarization. Gap junctional blockade in the peri-injection site simultaneously increased the amplitude and duration of the local [K]e response, and the local field response was greatly prolonged. While in the remote injection site, [K]e response was decreased after gap junctional blockage application. Optical stimulation decreased the [K]e both in the peri-injection and remote site. Our preliminary results are evidence of slow K redistribution (take for minutes) throughout the astrocytic syncytium which is partly mediated via astrocytic gap junctions. Potassium redistribution across a large area of the cortex is not a well-studied area because most studies have limited their focus on focal potassium dynamics. In this project we are addressing this gap using novel tools to elucidate potassium redistribution dynamics.