Biography:

Hong Jiang has completed her PhD from Qingdao University and Post-doctoral studies from Sun Health Research Institute. She is the Vice Dean, Medical College of Qingdao University. She has published more than 50 papers in reputed journals and has been serving as an Editorial Board Member of Current Alzheimer’s Disease.      
 

Abstract:

Some brain-gut peptides have been reported to have a close relationship with the central dopamine system. Nesfatin-1, a satiety brain-gut peptides co-expressed with ghrelin in X/A like endocrine cells in the gastric glands, has been reported exerted neuroprotective efficacy in center neurons system. Here we defined the neuroprotective effects of nesfatin-1 against MPTP-induced dopaminergic neuron degeneration in vivo and MPP+-induced cytotoxicity in vitro with its anti-apoptotic action via ameliorating mitochondrial dysfunction by activation of C-Raf/ERK1/2 pathway. In MES23.5 dopamingernic cells, nesfatin-1 pretreatment antagonized MPP+-induced mitochondrial dysfunction related apoptosis cascades including ΔΨm collapse, mitochondrion Cyt C releasing, caspase-3 activation and morphological changes of nuclei. This protective effect was abolished by selective inhibitor of C-Raf and ERK1/2. In C56BL/6 mouse, intracerebroventricular nesfatin-1 pretreatment attenuated MPTP-induced dopaminergic neuronal degeneration in the SNpc, dopaminergic fibers depletion, dopamine and its metabolites contents depletion in the striatum. Our data suggested nesfatin-1 had the potential to be considered as an agent for therapy of Parkinson’s disease.

Biography:

Ben Weinstock specializes in the rehabilitation of people with neurodegenerative diseases. He is the author of the only book about the prevention of Parkinson Diseases, “Preventing Parkinson’s: How to Cut Your Risk by Strengthening Your Multiple Shields” (2015). Another innovative approach that he has developed is EPIC-PD (Exercise Prescription, Individualized Care for Parkinson Diseases) which gives physical therapists a unique methodology for developing personalized lifestyle plans for each patient with PD. He also teaches continuing education seminars to undergraduate and post-doctoral physical therapists. He has completed his DPT from University of Montana City and continued his education at University of New York.        

Abstract:

Although detailed, individualized exercise prescriptions have been developed for a wide range of conditions, none have been developed for PD. Unfortunately, numerous cognitive errors have been woven into experimental designs of exercise and PD, including: Overlooking the heterogeneity of PD, leading to the assumption that PD is one disease; a lack of evaluating for PD mimics; the myth that PD is only a movement disorder, with the resulting failure to check for exercise-limiting non-motor dysfunctions (such as cardiac denervation); the belief that what is sound for healthy individuals will also work in a diseased state; the lack of awareness of the dangers of exercise in PD; and a failure to address other factors that influence exercise responses (such as circadian rhythms, medications, diet, sleep, etc.). EPIC-PD (Exercise Prescription, Individualized Care for Parkinson Diseases) overcomes these shortcomings by recognizing and applying cutting-edge research. This translational approach utilizes the evaluation of sensorimotor and autonomic responses to movement as well as through detailed questionnaires of medical and lifestyle factors. Exercise is recognized as the integration of motor and non-motor systems. The consistent application of critical clinical thinking is emphasized to determine when referrals need to be made to other members of the healthcare team, and when exercise should be halted to avoid exercise-induced dysfunctions. In summary, personalized exercise prescriptions and lifestyle management have the potential to maximize quality of life in persons afflicted with PD.

Biography:

Yu Zhou has completed her PhD from the Chinese Academy of Sciences (CAS), Shanghai Life Science Center and Postdoctoral training from Department of Neurobiology, University of California at Los Angeles (UCLA). She is currently appointed as a Full Professor in the Medical School of Qingdao University. Her research interests are focused on neurobiology of cognition and associated disorders. She has published more than 25 research papers in reputed neuroscience journals.  

Abstract:

Disrupted-in-schizophrenia 1(DISC1) is a promising candidate susceptibility gene for a spectrum of psychiatric illnesses that share cognitive impairments in common, including schizophrenia, bipolar disorder and major depression. Here we report that DISC1 L100P homozygous mutant shows normal anxiety- and depression-like behavior, but impaired object recognition which is prevented by administration of atypical antipsychotic drug clozapine. Ca2+ image analysis reveals suppression of glutamate-evoked elevation of cytoplasmic [Ca2+] in L100P hippocampal slices. L100P mutant slices exhibit decreased excitatory synaptic transmission (sEPSCs and mEPSCs) in dentate gyrus (DG) and impaired long-term potentiation in the CA1 region of the hippocampus. L100P mutation does not alter proteins expression of the excitatory synaptic markers, PSD95 and synapsin-1; neither does it changes dendrites morphology of primary cultured hippocampal neurons. Our findings suggest that the existence of abnormal synaptic transmission and plasticity in hippocampal network may disrupt declarative information processing and contribute to recognition deficits in DISC1 L100P mutant mice.  

Biography:

Prabaharan Chellamuthu is currently doing his Neurology residency in Institute of Neurology, Madras Medical College, Chennai, India. He has done his under graduation from 2004-2010 in Stanley Medical college, Chennai. He has done MD Paediatrics from 2011-2014 at Lady Hardinge Medical College, New Delhi, India. He has received Dr. C.B. Rama Rao prize and N. Radhakrishna Iyer prize in Stanley Medical College. He has published paper on infantile spasms and presented posters in both national and international conferences. His areas of interest are paediatric epilepsies and movement disorders.

Abstract:

Dystonia is a movement disorder characterized by sustained or intermittent muscle contractions causing abnormal, often repetitive, movements, postures, or both. The aim of the study is to present the profile of patients presenting with dystonia in a tertiary care center in southern India. The study period is from January, 2015 to June, 2016. Data of patients admitted in neurology ward or attending movement disorder clinic of Madras Medical College, Chennai, India were collected retrospectively and were analyzed. A total of 30 patients with dystonia were included in the study of which 43% (n=13) were males and the rest were females; 40% (n=12) patients had isolated dystonia while the remaining 60% (n=18) had combined dystonia syndromes. Based on the age of onset, 30% (n=9) patients had adolescent onset (13-20 yrs), 43% (n=13) had early adulthood onset (21-40 yrs) and 27% (n=8) had late adulthood onset (>40 yrs). Based on body distribution, 33% (n=10) patients had focal dystonia, 7% (n=2) had segmental, 47% (n=14) had multifocal dystonia, 7% (n=2) had hemidystonia and 7% (n=2) had generalized dystonia. Based on the etiology 47% (n=14) patients had degenerative cause [43% (n=13) cases had Wilson and 3% (n=1) had neuro acanthocytosis], 13% (n=4) patients had acquired cause [10% (n=3) cases were drug induced and 3% (n=1) due to hypoxic brain injury and in the remaining 40% (n=12) patients, no cause could be found. Based on the progression, 47% (n=14) patients had progressive disease and in the remaining patients the disease was static or recovered. Wilson’s disease is by far the common degenerative disease presenting with dystonia in our center & cervical dystonia is the most common idiopathic cause.

Biography:

Prabaharan Chellamuthu is currently doing his Neurology residency in Institute of Neurology, Madras Medical College, Chennai, India. He has done his under graduation from 2004-2010 in Stanley Medical college, Chennai. He has done MD Paediatrics from 2011-2014 at Lady Hardinge Medical College, New Delhi, India. He has received Dr. C.B. Rama Rao prize and N. Radhakrishna Iyer prize in Stanley Medical College. He has published paper on infantile spasms and presented posters in both national and international conferences. His areas of interest are paediatric epilepsies and movement disorders.

Abstract:

Dystonia is a movement disorder characterized by sustained or intermittent muscle contractions causing abnormal, often repetitive, movements, postures, or both. The aim of the study is to present the profile of patients presenting with dystonia in a tertiary care center in southern India. The study period is from January, 2015 to June, 2016. Data of patients admitted in neurology ward or attending movement disorder clinic of Madras Medical College, Chennai, India were collected retrospectively and were analyzed. A total of 30 patients with dystonia were included in the study of which 43% (n=13) were males and the rest were females; 40% (n=12) patients had isolated dystonia while the remaining 60% (n=18) had combined dystonia syndromes. Based on the age of onset, 30% (n=9) patients had adolescent onset (13-20 yrs), 43% (n=13) had early adulthood onset (21-40 yrs) and 27% (n=8) had late adulthood onset (>40 yrs). Based on body distribution, 33% (n=10) patients had focal dystonia, 7% (n=2) had segmental, 47% (n=14) had multifocal dystonia, 7% (n=2) had hemidystonia and 7% (n=2) had generalized dystonia. Based on the etiology 47% (n=14) patients had degenerative cause [43% (n=13) cases had Wilson and 3% (n=1) had neuro acanthocytosis], 13% (n=4) patients had acquired cause [10% (n=3) cases were drug induced and 3% (n=1) due to hypoxic brain injury and in the remaining 40% (n=12) patients, no cause could be found. Based on the progression, 47% (n=14) patients had progressive disease and in the remaining patients the disease was static or recovered. Wilson’s disease is by far the common degenerative disease presenting with dystonia in our center & cervical dystonia is the most common idiopathic cause.

Biography:

Matteo Santoro was born in 1988 in south of Italy. He is currently working on Parkinson’s disease and investigating the role or a protein called HMGB1 in the pathophysiology of the disease. During his PhD Matteo Santoro has received four different prizes for best PhD student poster presentation and talks at different conferences within and outside the University of Aberdeen. He successfully co-authored two peer reviewed research articles on Parkinson’s disease. The latest publication has seen him the main contributor of the study. He is currently working as PhD student on the behavioural characterization of three different MPTP mouse models of Parkinson’s disease and investigating the role of acquired and innate immune system in Parkinson’s disease.

Abstract:

Background: High-mobility group box 1 (HMGB1) is a nuclear and cytosolic protein that is released during tissue damage from immune and non-immune cells – including microglia and neurons. HMGB1 is implicated in the progression of numerous chronic inflammatory and autoimmune diseases. There is increasing evidence from in vitro studies that HMGB1 may link the two main pathophysiological components of Parkinson’s disease (PD), i.e. progressive dopaminergic cell degeneration and chronic neuroinflammation both of which underlie the mechanistic basis of PD progression.

Materials & Methods: Pharmacological trials - Male mice C57BL6J ten weeks old were randomly divided in four experimental groups (n=5 per group). i) saline control group, ii) MPTP treated groups (sub-acute regimen 30 mg/kg of MPTP intraperitoneally (i.p.) once a day for five consecutive days), iii) MPTP treated group plus i.p. dose of 50mg/kg glycyrrhizin, iv) MPTP treated group plus i.p. dose of 200 ug HMGB1 neutralizing antibody. HMGB1 nuclear translocation was assessed in mice and human brain tissue via co-immunolocalization in three different nigral cell populations: tyrosine hydroxylase (TH) positive neurons, microglia and astrocytes. Western blotting was performed on protein samples extracted from ventral midbrain.

Results: In a mouse model of PD induced by sub-acute administration of 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) the small natural molecule glycyrrhizin, a component from liquorice root which can directly bind to HMGB1, both suppressed MPTP-induced HMGB1 and RAGE upregulation while reducing MPTP-induced dopaminergic cell death in a dose dependent manner.

Conclusion: HMGB1 serves as a powerful bridge between progressive dopaminergic neurodegeneration and chronic neuroinflammation in a model of PD, and suggest that HMGB1 is a suitable target for neuroprotective trials in PD.

Biography:

Matteo Santoro was born in 1988 in south of Italy. He is currently working on Parkinson’s disease and investigating the role or a protein called HMGB1 in the pathophysiology of the disease. During his PhD Matteo Santoro has received four different prizes for best PhD student poster presentation and talks at different conferences within and outside the University of Aberdeen. He successfully co-authored two peer reviewed research articles on Parkinson’s disease. The latest publication has seen him the main contributor of the study. He is currently working as PhD student on the behavioural characterization of three different MPTP mouse models of Parkinson’s disease and investigating the role of acquired and innate immune system in Parkinson’s disease.

Abstract:

Background: High-mobility group box 1 (HMGB1) is a nuclear and cytosolic protein that is released during tissue damage from immune and non-immune cells – including microglia and neurons. HMGB1 is implicated in the progression of numerous chronic inflammatory and autoimmune diseases. There is increasing evidence from in vitro studies that HMGB1 may link the two main pathophysiological components of Parkinson’s disease (PD), i.e. progressive dopaminergic cell degeneration and chronic neuroinflammation both of which underlie the mechanistic basis of PD progression.

Materials & Methods: Pharmacological trials - Male mice C57BL6J ten weeks old were randomly divided in four experimental groups (n=5 per group). i) saline control group, ii) MPTP treated groups (sub-acute regimen 30 mg/kg of MPTP intraperitoneally (i.p.) once a day for five consecutive days), iii) MPTP treated group plus i.p. dose of 50mg/kg glycyrrhizin, iv) MPTP treated group plus i.p. dose of 200 ug HMGB1 neutralizing antibody. HMGB1 nuclear translocation was assessed in mice and human brain tissue via co-immunolocalization in three different nigral cell populations: tyrosine hydroxylase (TH) positive neurons, microglia and astrocytes. Western blotting was performed on protein samples extracted from ventral midbrain.

Results: In a mouse model of PD induced by sub-acute administration of 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) the small natural molecule glycyrrhizin, a component from liquorice root which can directly bind to HMGB1, both suppressed MPTP-induced HMGB1 and RAGE upregulation while reducing MPTP-induced dopaminergic cell death in a dose dependent manner.

Conclusion: HMGB1 serves as a powerful bridge between progressive dopaminergic neurodegeneration and chronic neuroinflammation in a model of PD, and suggest that HMGB1 is a suitable target for neuroprotective trials in PD.

Biography:

Benjamin E Aghoghovwia has completed his MSc from the University of Lagos, Nigeria. He is currently near the end of the second year of his PhD at the Department of Anatomy and the Brain Health Research Centre, University of Otago, Dunedin, New Zealand. He has published 3 papers in reputed journals, including the Journal of Anatomy, and has been serving as a Laboratory Demonstrator in undergraduate courses on neuroscience and health sciences at the University of Otago

Abstract:

Hypoxic-ischemic (HI) brain injury can cause disabilities in term-born infants. This study investigated the therapeutic effects of adult-sourced adipose-derived mesenchymal stem cells (MSCs) on motor skills, and on neuronal restoration in the anterior striatum, following HI-induced brain injury. On postnatal day (PN) 7, Sprague-Dawley rat pups were exposed to HI right-sided brain injury, weight-matched and assigned to groups (n=8-10/group)–untreated (HI+Dil), normal controls (Normal+Dil), single stem cell-treated (HI+MSCs×1) and double stem cell-treated (HI+MSCs×2). On PN14 and 16, all groups were treated with either diluent or stem cells. All animals were then tested repeatedly on the cylinder and staircase tests for their motor skill ability and perfused on PN106/107. Serial 5 µm thick frozen sections were cut coronally through the brain using a cryostat and immunohistochemically stained for striatal dopamine- and cAMP-regulated phosphoprotein-32-positive spiny projection neurons. The absolute number of these neurons was estimated using the Cavalieri’s, physical dissector and Abercrombie/unfolding methods. HI groups were significantly impaired on left- versus right-sided motor skills on the staircase test (e.g. HI+MSCs×1, repeated ANOVA, p<0.005), but the control animals were not. The absolute number of DARPP-32-positive neurons in the striatum was significantly greater (Student’s t-test, p<0.04) in the control group compared to all HI groups. There was no statistically significant rescue of motor skills or striatal spiny projection neurons by delayed single- or double-treatment with adipose-derived MSCs. These results suggest that treatment with this particular type of stem cell has limited therapeutic potential for rescuing striatal neurons and motor deficits after neonatal hypoxia-ischemia.