9^th Global Neuroscience Conference November 21-22, 2016 Melbourne, Australia

Biography:

Saman Azizi has completed his  M.D degree at the age of 26 years from Shiraz University of Medical science. He has published his paper in Global Journal of Health Science in the field of psychiatry with head of psychiatry department and He is working on 2 papers now.

Abstract:

Biography:

Dr Tayebi is a Senior academic at the University of Melbourne and heads the protein misfolding disease group. Dr Tayebi has previously very successfully led to satrt up biotechnology companies in the UK and the US.

Abstract:

An active and promising area of research for Alzheimer’s disease (AD) is immunotherapy using antigens (active) or antibodies (passive) that target AD neuropathology. Senile plaques contain the beta-amyloid (Aβ) peptide that is derived from a longer precursor protein, amyloid  precursor protein. Amyloid beta is produced as either a 40 or 42 amino acid peptide, the latter being more fibrillogenic and toxic than the shorter isoform. Initially produced as a soluble peptide, Aβ subsequently can form oligomers, a molecular complex of monomer units. Aβ oligomers are highly toxic to neurons and particularly damaging to synapses. There is strong evidence that oligomer accumulation may seed plaque aggregation and serves as an early molecular target for preventing AD. Interestingly, oligomers can be detected by antibodies based upon structure with less of a need to target the amino acid sequence of an individual protein making antibody development for oligomers a fascinating area to pursue. Antibodies developed against oligomers may be able to bind several misfolded proteins implicated in neurodegenerative diseases.

Immunotherapy studies have typically used transgenic mouse models of AD, and subsequently translated to human clinical trials. However, the success rate of these translational studies has been limited. In contrast, studies in another animal model, the aged canine, indicated that immunotherapy led to similar outcomes in AD clinical trials; reduced Aβ plaque pathology with no improvements in cognition but indications of a slowing of cognitive decline.

We have previously developped and chatacterized unique anti-Aβ single domain antibodies derived from camelids. These antibidies, we called PRIOAD, were able to (i) cross the in vitro and in vivo blood brain brain (BBB) in mice rats and in vitro human BBB model; (ii) bind with high affinity to soluble oligomers derived from synthetic and native human Aβ but not their monomeric and fibrils counterparts; and (iii) not induce neurotoxic effects and host mmune responses in mice.

PRIOADs were evaluated for their therapeutic efficacy in a pilot sutdy using aged beagles with  mild cognitive imparement. Following intraventricular infusion of PRIOAD for 3 months, there was a significant reduction of Aβ plaque burden in these animals. More importanly, PRIOADs led to reversal of the cognitive deficits in beagles.

The study was very encouraging and will be expanded to include larger number of animal cohorts prior to translation into human clinical trials.

Biography:

Majid Gharghani is one of the postgraduate pioneer students in field of neuroimmunology and neural stem cell culture. He has worked as a research and teaching assistant at the age of 25 years in Yasuj university of medical sciences, Iran. He also has attended several workshops to enhance his practical understanding of various in vivo and in vitro techniques including immunohistochemistry, immunofluorescence, neural stem cell culture and EAE models.

Abstract:

Multiple sclerosis (MS) is associated with a neuropsychiatric problems of which depression is the commonest. Also, antidepressant drugs are known to impact on the immune system and CNS cells. Aim of present study was to introduce an antidepressant drug with ameliorative effects on experimental autoimmune encephalomyelitis (EAE) severity, an animal model of MS, including spinal cord inflammation and demyelination.

In this study, the protective effect of fluvoxamine, a selective serotonin reuptake inhibitor (SSRI), was investigated in cultured cultured embryonic neural stem cells (ENSCs) and rat model of acute EAE. First, we examined the effect of fluvoxamine on proliferation and differentiation of cultured ENSCs. Next, it’s immunomodulatory and oligodendrogenesis properties was investigated in EAE model of Lewis rats.

Results showed that fluvoxamine increases the viability and proliferation of ENSCs. Moreover, treatment of NSCs by fluvoxamine resulted in a significant increase in diferentation toward oligodendrocyte cells (MBP possitive cells) and also astrocyte cells (GFAP positive cells). IN vivo results of EAE rats, demonstrated that clinical outcomes of EAE were ameliorated in fluvoxamine- versus PBS-treated EAE rats. Fluvoxamine caused a significant decrease in serum IFN-γ, in comparison to PBS-treated EAE rats, while significantly increased serum IL-4 level. Furthermore, histopathological observations showed statistically decreased lymphocyte infiltration with no demyelinated surface area in the lumbar spinal cord of fluvoxamine-treated, in comparison to PBS-treated EAE rats. Finally, immunofluorescent analysis clearly showed decrease in number of activated astrocytes (GFPA positive cells) and increase in area of mature oligodendrocyte (MBP positive cells) in fluvoxamine treated EAE groups, in comparison to PBS treated EAE rat.

In conclusion, for the first time, our results indicated a positive impact of fluvoxamine on proliferation and differentiation of cultured ENSCs. Moreovere, high potential of fluvoxamine in EAE improvment was confirmed by indication its anti-inflammatory and oligodendrogensis activies. Our data suggest that fluvoxamine could be one of the antidepression drugs in MS patient with anti-inflammatory and remyelination effects, which needs further clinical studies.

Biography:

Shivam Bansal is presently an undergraduate (final year) student at the premier institute, AIIMS, New Delhi. He is a topper in the institute and has been awarded medal and certificate for obtaining highest marks in the subject of Biochemistry and Microbiology. Apart from academic work, he is active in research in the Dept. of Neurology under Prof. Achal Srivastava (well acclaimed in the field of headache, ataxia, intractable epilepsies and spinal cord disorders) as the guide. The above mentioned research was also selected for oral presentation at annual convention of Aiimsonians of America (AoA) at Daytona Beach, Florida. 

Abstract:

Background:

Studies suggest a degree of autonomic dysfunction which gets implicated in pathophysiology of migraine but none has ever commented on differences among ictal and interictal (headache free) period of migraine. Therefore this pilot study aims at assessing and comparing autonomic function during ictal and interictal period.

Methods and Materials:

Patients with migraine according to ICHD 3^rd edition β version criteria were recruited for the study. Tests of sympathetic function (beat to beat blood pressure changes in Head-Up-Tilt test) and parasympathetic function (heart rate responses to Deep Breathing and Valsalva Manoeuvre) were performed, each during ictal and interictal period. The results of the ictal period were then compared with that of interictal period.

Results:

Ten patients [Eight female (80%), 20-58 years, mean 34.6] were studied. Nine patients (90%) showed Expiration:Inspiration [E:I] ratio {Ratio of maximum RR interval during expiration phase with minimum RR interval during inspiration phase} in Deep Breathing test below 1.24 and four patients (40%) showed 30:15 ratio {Ratio of RR interval during 30^th heart beat with that during 15^th heart beat} in Head-Up-Tilt test below 1.04, thus indicating significantly higher vagal response. These results were in ictal period. All patients exhibited normal parasympathetic response during interictal period and intact sympathetic function during both ictal and interictal periods.

Conclusion:

Subjects with migraine had vagal hyperactivity and intact sympathetic function during ictal period, whereas no abnormality was found during headache free period. This study provides newer insight into the pathophysiology of a migraine attack which may lead to further studies with new therapeutic approaches.

Biography:

Son CG graduated Oriental Medical Collage of Daejeon University, and then  had finished a clinical training course for internal medicine specialist in Daejeon Oriental Hospital, and PhD degree in Daejeon University. He had studies in oncology branch, NCI, NIH, USA as a post-doctoral fellow from 2002 to 2004. Currently he is a professor and director of Institute of Traditional Medicine & Science, Daejeon University. He has focused his research on a broad range of Traditional Oriental medicine in both laboratory and clinical studies.

Abstract:

We evaluated the neuropharmacological effects of Gongjin-Dan (GJD) on the memory impairment caused by scopolamine injection. BALB/c mice were orally treated with GJD (100, 200, or 400 mg/kg, daily) or tacrine (THA, 10 mg/kg) for 10 days, and scopolamine (2 mg/kg) was injected intraperitoneally. The radial arm maze and passive avoidance tests were performed to evaluate the animal’s learning and memory. Scopolamine increased the time to complete the task, the number of total errors (reference and working memory error) in the radial arm maze task, and the latency time in the passive avoidance test, which were significantly ameliorated by treatment with GJD. The GJD treatment also ameliorated the scopolamine-induced hyperactivation of acetylcholinesterase activity, and suppression of the expression of brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF) and their receptors in the hippocampus. These effects of GJD were supported by both the doublecortin (DCX)-positive staining, which was used to detect hippocampal neurogenesis, and Nissl staining, which was used as a measure of hippocampal atrophy. These findings strongly suggest that GJD exerts a potent anti-amnesic effect, and its underlying mechanism might involve the modulation of cholinergic activity.

Biography:

Binna Kim is a PhD candidate in the Interdisciplinary Program in Brain Science at Seoul National University, South Korea. She is also a researcher at Ewha Brain Institue. She received her BS in chemistry and BA in psychology from the SNU in 2011. Binna Kim was granted Global PhD Fellowship scholarship from National Research Foundation of Korea, and participated in several projects as well. Her current research interests include cognitive and social neuroscience.

Abstract:

Recent advance in computational analysis of multimodal neuroimaging using machine learning algorithms may enable early diagnosis of central nervous system diseases and predict the subsequent prognosis with high accuracy. In the current study, disaster survivors who were diagnosed with posttraumatic stress disorder (PTSD) in the early aftermath of trauma and healthy individuals who were not exposed to trauma were followed up as the trauma-exposed and trauma-unexposed groups prospectively. We assessed the multimodal characteristics of the fear circuitry’s brain regions including the amygdala, ventral prefrontal cortex, and hippocampus with volume, connection density, connection cost, tract strength, and network efficiency as variables associated with brain regions. Using a classification approach with multimodal neuroimaging data for an analysis, features of particular subset brain regions - the amygdala, ventral prefrontal cortex, hippocampus, insula, and thalamus - were identified to best characterize those of trauma-exposed group. We found that amygdalar volumes and the tract strength of its connections in combination with the insula and with the thalamus each were robust brain classifiers for the trauma-exposed group during an early stage of post-trauma when most of the survivors still meet the diagnostic criteria for PTSD. In contrast, the tract strength of the amygdala-ventral prefrontal cortex connection was a differentiating feature of the trauma-exposed group from that of the trauma-unexposed group during the recovery period from PTSD. These results suggest that the use of multimodal imaging analysis may applied as a competent and efficient tool in PTSD risk prediction.

Biography:

Shivam Bansal is presently an undergraduate (final year) student at the premier institute, AIIMS, New Delhi. He is a topper in the institute and has been awarded medal and certificate for obtaining highest marks in the subject of Biochemistry and Microbiology. Apart from academic work, he is active in research in the Dept. of Neurology under Prof. Achal Srivastava (well acclaimed in the field of headache, ataxia, intractable epilepsies and spinal cord disorders) as the guide. The above mentioned research was also selected for oral presentation at annual convention of Aiimsonians of America (AoA) at Daytona Beach, Florida. 

Abstract:

Background:

Studies suggest a degree of autonomic dysfunction which gets implicated in pathophysiology of migraine but none has ever commented on differences among ictal and interictal (headache free) period of migraine. Therefore this pilot study aims at assessing and comparing autonomic function during ictal and interictal period.

Methods and Materials:

Patients with migraine according to ICHD 3^rd edition β version criteria were recruited for the study. Tests of sympathetic function (beat to beat blood pressure changes in Head-Up-Tilt test) and parasympathetic function (heart rate responses to Deep Breathing and Valsalva Manoeuvre) were performed, each during ictal and interictal period. The results of the ictal period were then compared with that of interictal period.

Results:

Ten patients [Eight female (80%), 20-58 years, mean 34.6] were studied. Nine patients (90%) showed Expiration:Inspiration [E:I] ratio {Ratio of maximum RR interval during expiration phase with minimum RR interval during inspiration phase} in Deep Breathing test below 1.24 and four patients (40%) showed 30:15 ratio {Ratio of RR interval during 30^th heart beat with that during 15^th heart beat} in Head-Up-Tilt test below 1.04, thus indicating significantly higher vagal response. These results were in ictal period. All patients exhibited normal parasympathetic response during interictal period and intact sympathetic function during both ictal and interictal periods.

Conclusion:

Subjects with migraine had vagal hyperactivity and intact sympathetic function during ictal period, whereas no abnormality was found during headache free period. This study provides newer insight into the pathophysiology of a migraine attack which may lead to further studies with new therapeutic approaches.

Biography:

Borovok Natalya has completed her PhD at the age of 34 years from Institute of Chemical Physics, Russian Academy of Sciences, Moscow, Russia and postdoctoral studies from Tel-Aviv University, Department of Biochemistry, Israel. She is the senior researcher of the Department of  Biochemistry and Molecular Biology, Tel-Aviv University . She has published more than 30 papers in reputed scientific journals.

Abstract:

Background: Serine/threonine kinase AKT/PKB plays a fundamental role in a wide variety of neuronal functions, including neuronal cell development, axonal growth and synaptic plasticity. Recently, a further downstream mechanism of AKT involvement in long-term depression (LTD) prevention and late phase long-term potentiation (LTP) has been revealed. However, no solid knowledge has been accumulated regarding the downstream effectors mediating AKT’s effects on early phase LTP (eLTP). Aim: elucidating of the role of AKT in eLTP regulation. Results: Using different regimes for application of the AKT inhibitor A6730 (30 min drug exposure before high frequency stimulation (HFS), drug for 30 min before and 20 min after HFS, drug for 20 min 30 min after HFS), to acute hippocampal slices trained with the HFS paradigm, we observed that AKT regulates LTP induction and expression without affecting its maintenance. Further, we delivered an AKT activator to combine with inhibitors of various signaling pathways to prevent AKT activation-induced effect on LTP and to characterize a potential downstream mechanism of LTP regulation. Unexpectedly, SC79 (activator of AKT), which also prevents AKT translocation to the plasma membrane, induced a significant decrease in basal synaptic activity and in expression of LTP. Conclusions: 1) translocation of AKT towards the plasma membrane is necessary for regulation of synaptic activity and LTP. 2) AKT related LTP expression is not dependent on downstream cytosolic factors, but is mediated via direct effects of AKT on post-synaptic density components and glutamate receptors.