17^th Global Neuroscience Conference October 16-17, 2017 Osaka, Japan

Biography:

Takakazu Yokokura has his expertise in genetics and molecular biology and passion in finding approaches to cure devastated neurological disorders, such as spinal muscular atrophy (SMA) and amyotrophic lateral sclerosis. Animal model that he and his colleague established for SMA study, which is established in invertebrate, has shed light on gene networks Survival Motor Neuron (SMN) gene is integrated in. His study has focused on elucidate underlying molecular mechanisms that low levels of SMN leads to manifestation of SMA neuromuscular pathological phenotypes.

Abstract:

Spinal Muscular Atrophy (SMA) is a devastating inherited disorder characterized by progressive loss of motor activity, failure of neuromuscular synapses and muscle weakness. Genetic cause of SMA is mutation of Survival Motor Neuron 1 (SMN1) gene, while genetic factor determining severity of symptom is copy number of Survival Motor Neuron 2 (SMN2) gene, which only generate small amount of SMN protein due to skipping a functionally important exon at high frequency. As SMN has been considered as a key factor to regulate neuronal cell function cell autonomously, up-regulating SMN protein in spinal cord motor neurons at pre-symptomatic stages is the most advanced therapeutic approaches to prevent, or, at least, delay irreversible loss of motor neurons. However, the fact that SMA patients exhibit muscle weakness and experience fatigue suggests that it is little known underlying mechanism how low SMN levels affect to trans-synaptic biology at the neuromuscular junction (NMJ). Trans-synaptic structure and signaling at the NMJ play important roles for establishment and maintenance of neuromuscular connectivity and functions. As pathological observation in post-mortal NMJ specimen or rodent SMA models exhibited abnormality in neuromuscular connectivity, utilizing Drosophila NMJ, which is well characterize its structure and molecular mechanism, allow us to understand how low levels of SMN perturbs structure and molecular mechanism at the NMJ in depth. Severe SMN mutants exhibited two phenotypes in motor unit known as SMA pathology, loss of motor axon and abnormality at the NMJ. Modulation of trans-synaptic two canonical signaling pathways, BMP and FGF signaling, that have shown genetic interaction to SMN, can rescue the SMN defects. In addition, each pathway seems to modulate distinct aspect of SMA motor unit pathology.

Biography:

Nikki Stang was born in Denver, Colorado. In 2007 she attended UNLV to start a psychology degree. Shortly after attending college she moved to Peru where she volunteered in an all girls orphanage. She developed a passion for working with children and eventually found her calling in being a gym teacher for high risk youth in the city of Denver. In 2011 she began attending massage school to learn more about the body and how she personally could help people around the world who did not have access to medical care. In fall of 2011 she was accidentally headbutted in the mouth and suffered a traumatic brain injury while playing basketball with her students. Nikki was unaware of her TBI until 2013 when she was later diagnosed shortly after she was pregnant with her first child. Nikki has recovered from her accident and is now and advocate for brain injury survivors. She has taken classes in aromatherapy and healing touch through ISHA, craniosacral therapy through the Upledger Institute, and heart centered therapy through the Chikly Health Institute. She is currently living in Denver with her two young children and is a TBI advocate, motivational speaker, and is working on writing a book about her traumatic brain injury experiences. 

Abstract:

CranioSacral Therapy is an International Program which is taught and ran through the Upledger Institute. www.upledgerinstitute.com

Craniosacral Therapy (CST) was invented by osteopathic physician John E. Upledger when he was a Professor of Biomechanics at Michigan State University.  Following extensive scientific research he found that by using a very soft-touch therapy (about 5 grams of pressure), restraints are released in the the craniosacral system, which is comprised of membranes and fluid that surround and protect the brain and spinal cord. CST can support the body’s natural healing process as well as serve as a preventative health measure for a diverse range of health problems and neurological dysfunction including concussion, Traumatic Brain Injury, Alzheimer's and Dementia, and Central Nervous System Disorders. Nikki Stang will talk about her personal experience with TBI including the symptoms she was experiencing and how implementing CranioSacral Therapy with other modalities eliminated many of the symptoms associated with TBI that she was experiencing. CranioSacral Therapy has proven to be effective in increasing function and decreasing pain associated with head trauma. 

Biography:

Joshua has his PhD in Anatomy and Neuroscience and MBA with specialisation in Clinical Research Management. He currently works as a teacher and researcher in the Ben Carson [Snr.] College of Medicine, Babcock University, Nigeria. His working motto is: Becoming a professional of the best quality; serving my organization with absolute sincerity, commitment and positive passion to achieve a collective purposeful objective; impacting humanity positively and making the world a better place

Abstract:

This study investigated the effects of caffeine consumption on the brain  in pregnancy and early postnatal life. Thirty two (n=32) adult mice (Mus musculus) were used for the study. They were maintained in Anatomy Department animal holding and given chow and water ad libitum. They were divided into four groups: Group A animals as control; Group B animals given low-dose caffeine- 10mg/kg body weight; Group C animals given medium-dose caffeine- 50mg/kg body weight; and Group D animals given high-dose caffeine- 120mg/kg body weight. The treatment duration was divided into Phases I and II to assess pre- and postnatal effects respectively. Caffeine was dissolved in distilled water and Group A received distilled water as placebo. Animals mated prior to treatment commencement and pregnant mice were administered caffeine throughout pregnancy. Half number of offspring were sacrificed at birth; the rest were used in Phase II and treatment continued till postnatal Day 35, marking puberty. Animals were sacrificed and brain specimens were excised and processed.  Specimens were subjected to gross morphological assessments. Histological and histochemical demonstrations were done using the H&E, Bielschowsky, Luxol Fast Blue and Feulgen DNA Staining techniques. Immunohistochemical-molecular properties were demonstrated using the GFAP technique.  At parturition, 50mg/kg body weight caffeine dose disrupted deeper cortical layers histoarchitecture and extended to other layers when dosage increased to 120mg./kg body weight. Neuronal morphological heterogeneity was observed at doses higher than 10mg/kg body weight and some effects persisted till puberty. Astrocyte morphologies and dendritic patterns of elaboration were persistently altered. Caffeine exposure altered the pattern of brain cells development by altering morphologies, patterns of elaboration and spatial distribution; also neuronal communication and basal metabolism. Effects were dose dependent and moderate dose might be beneficial to morphological and functional parameters.  

Biography:

Arash Abdolmaleki has his expertise in peripheral nerve regeneration. His PhD thesis was about the use of acellular nerve scaffolds enriched by bone marrow mesenchymal stem cells for enhance the regeneration of sciatic nerve after implantation in rats. 

Abstract:

Acellular nerve graft is an alternative to autograft for the repair of short gaps associated with peripheral nerve injury. It provides a suitable three-dimensional structure that supports and guides axonal regeneration. However, outcomes associated with the use of acellular nerve grafting are often inferior to those achieved with autografts, particularly over long lesion gaps. Therefore, this experimental study was conducted to evaluate the effects of citicoline on the efficacy of acellular nerve allografts seeded with bone marrow stem cells (BMSCs) to bridge a 15-mm sciatic nerve gap. Seventy rats were randomly allocated into seven groups (n = 10 per group), including the healthy control group, sham surgery group, autograft group, acellular nerve scaffold (ANS) group, ANS + BMSCs group, ANS + BMSCs + 100 mg/kg citicoline, and ANS + BMSCs + 200 mg/kg citicoline groups. The two experimental groups were treated daily with citicoline at the doses of 100 or 200 mg/kg for two weeks. After implantation, motor function was assessed and electrophysiological, histomorphometry, and molecular tests were performed. Animals treated with citicoline immediately after implantation showed significantly better regeneration and motor function outcome compared with ANS group, and ANS + BMSCs group. No significant difference was observed between the citicoline treatment (200 mg/kg) group and the autograft group. These findings suggest that citicoline treatment resulted in improved regenerative properties of cell-seeded nerve allografts, likely via increasing the viability and retention of transplanted BMSCs

Biography:

Abstract:

The Astrocytic proliferation following chronic consumption of thermoxidized and fresh palm oil diets was studied on the brainstem of growing mice. Thirty mice were divided into three groups A, B and C. 15g of thermoxidized palm oil was mixed with 85g of mice chow (15%w/w) and given to the group C animals. 15g of fresh palm oil was mixed with 85g of mice chow (15% w/w) and administered to the group B animals while group A animals were fed with normal mice chow. The astrocytes in the brainstem of mice in the thermoxidized palm oil group significantly increased in number (Hyperplasia) and size (Hypertrophy) when compared with animals in the control and fresh palm oil groups due to the presence of concomitant evolution of toxic bye-products (free radicals, peroxides etc ). If the results obtained in mice are applicable to man, there is reason for concern regarding adverse consequences of chronic consumption of thermoxidized palm oil diet. This may be dangerous to health since it may result in Astrocytic proliferation in brainstem, thereby making the animals susceptible to loss of motor function like control of cardiovascular system, respiration, gastrointestinal tract, eye movement, etc.

Biography:

Seiju Kobayashi was born on March 11, 1976 in Japan. Presently Holding a position of Director in department of Psychiatry and Medicine at Nakae Hospital From 2001-2002 worked at Department of Neuropsychiatry, Sapporo Medical University School of Medicine, Sapporo, Japan, 2002-2003: Department of Psychiatry, Goryokai Hospital,  2003-2004: Department of Neuropsychiatry, Sapporo Medical University School of Medicine, Sapporo, Japan,  2004-2008: Department of Psychiatry, Sunagawa City Medical Center, Sunagawa, Japan,  2008-2016: Department of Neuropsychiatry, Sapporo Medical University School of Medicine, Sapporo, Japan , 2017 : Nakae Hospital.

Abstract:

Current diagnostic criteria recommend neuroimaging as a diagnostic support tool for the clinical diagnosis of dementia with Lewy bodies (DLB). Because DLB causes characteristic impairments and disabilities, such as neuroleptic hypersensitivity, which may significantly increase morbidity and mortality, its prompt and correct diagnosis is very important. The aim of this study was to evaluate the extent with which diagnostic accuracy can be increased using a combination of brain perfusion SPECT (bp-SPECT), 123 I-metaiodobenzylguanidine myocardial scintigraphy (MIBG scintigraphy), and DAT-SPECT. Taking finances and patient burden into consideration, we compared the tests to determine priority.

Methods: Thirty-four patients with probable DLB (75.0 ± 8.3 years old, 14 male: 20 female) underwent bp-SPECT, MIBG myocardial scintigraphy, and DAT-SPECT.

Results: Our comparison of three functional imaging techniques indicated that MIBG scintigraphy (79%) or DAT-SPECT (79%) had better sensitivity for characteristic abnormalities in DLB than bp-SPECT (53%). The combination of the three modalities could increase sensitivity for diagnosis of DLB to 100%. Additionally the ratio of patients with rapid eye movement sleep behavior disorder (RBD) was significantly higher in MIBG (+) group than in MIBG (-) group.

Conclusions: In the stand-alone diagnostic means, priority should be placed on MIBG scintigraphy or DAT-SPECT for the diagnosis of DLB. However, our results suggest that the combination of bp-SPECT, MIBG scintigraphy, and DAT-SPECT increased accuracy of the clinical diagnosis of DLB.

Biography:

Chun-Wei Hsu is doing her Ph.D. in Psychology at University of Plymouth since April 2014. She went to undergraduate school at National Taiwan University, and double majored in life science and psychology within four years (Sep. 2007 – Jun. 2011). Later, she completed a master’s degree in Cognitive Neuroscience and Human Neuroimaging at University of Sheffield (Se. 2012 – Aug. 2013). Currently, her Ph.D. project is to explore the cognitive mechanisms underlying deception through creativity and neuroscience. Chun-Wei is interested in how people conduct high-level cognition in complex social interaction and how people evaluate expect the pay-offs and take action during the decision-making process. Ideal interaction requires people to simulate others' perspectives and shape their behaviors, which is of great interest to her. Human neuroimaging methods with fMRI or EEG are the approach she wants to use to answer my research questions.

Abstract:

Concealed information paradigms (CITs) have been developed to determine if an individual is familiar with a certain piece of information such as a crime-related item. The main logic of CITs is that recognition of an item of interest (probe) will generate a differential response, compared to suitable control items (irrelevants) that can be detected by monitoring behavioral, psychophysiological, or neural variables.

An important issue is an extent to which countermeasures used by suspects can reduce the accuracy of the CIT. Recent work has focused on neural variables measured with functional magnetic resonance imaging (fMRI) because at first sight, such variables may seem more resistant to countermeasures than more peripheral variables. Previous work has shown that hybrid physical and mental countermeasures can decrease the accuracy of fMRI-based CITs, but questions remain as to whether purely mental countermeasures can do so as well. Existing evidence shows that attentional and memory strategies can decrease the accuracy with which one can use fMRI to detect successful recognition in standard face recognition tasks.

The aim of this fMRI study was to determine if such mental countermeasures are effective also with standard CITs. Participants (N=20) were tested under three conditions: no knowledge, concealed knowledge, and countermeasures. Results based on regions of interest defined in previous CIT studies showed that the area under the curve (AUC) for discriminating no knowledge and concealed knowledge cases with multi-voxel pattern analyses was 0.86 without countermeasures. Critically, memory and attentional countermeasures significantly reduced the AUC to 0.74.

These results indicate that purely mental countermeasures can reduce the accuracy of fMRI-based CITs, even without extensive training of participants.

Biography:

Jarren Mae R. Escape has completed her Doctor of Medicine degree at the age of 24 years old from University of Santo Tomas. She finished her three-year residency training in Pediatrics at Makati Medical Center.

Abstract:

Febrile seizures (FS) occur in 4-5% of children and account for the majority of seizures seen in children in emergency rooms. Local clinical practice guidelines for FS were developed in 2004. We undertook this study to look at the demographic profile of children admitted with FS, review their clinical course, diagnostic evaluations, drug management, etiology of fever, and neurological outcome.  It is our hope that the information gained from this study would aid in the revision and adaptation of local clinical practice guidelines for FS.  Objective: To describe the clinical profile, fever etiology, clinical course, diagnostics and neurological outcome of patients admitted with febrile seizures.  Data gathered was compared with clinical practice guidelines. Methodology: Retrospective descriptive study that reviewed hospital records of children admitted with febrile seizures over 7 years. Results: A total of 373 patients comprised the sample population. Eighty-nine percent were simple febrile seizures.  Ages ranged from 3 to 91 months with the largest group in the 13-18 month old range.  There was male preponderance and higher number of admissions during the rainy season. Family history was common, paternal side dominant.   The most common cause of fever was upper respiratory tract infection and systemic viral Illness. CBC was done in all patients.  EEG’s were done in 27.35% of patients; 41 % done in simple febrile seizures.  Intravenous fluids and antipyretics were given and diazepam was ordered in all patients; antibiotics were given to 62.2 % of patients.  Patients with complex febrile seizure are more likely to be referred to subspecialist and/or have more laboratory and imaging tests.  Neurological outcome was normal. Conclusion: This study showed male preponderance, increased paternal family history and seasonal variation in FS.  In spite of upper respiratory tract infection and systemic viral diseases being the most common cause of fever, majority of patients received antibiotics.  There was noted deviation from approved clinical practice guidelines.

Biography:

Nargol Ahmadi-Mahmoodabadi is a PhD in Cognitive Neuroscience. Her research and practice areas of interest are Behavioral neuroscience, Learning and memory and Behavioral neurophysiology.

Abstract:

This study performed to investigate the influence of bilateral post-training intra-prelimbic (PL) microinjections of serotonergic 5-HT4 receptor agents (RS67333, as a 5-HT4 receptor agonist and RS23597-190, as a 5-HT4 receptor antagonist ) upon amnesia induced by a cannabinoid CB1 receptor agonist, arachidonylcyclopropylamide (ACPA) in rats. The step-through inhibitory avoidance (IA) and open filed apparatuses were used to examine the memory consolidation and locomotion behaviors, respectively. Bilateral guide-cannulae were implanted to allow intra-PL microinjections of the drugs. Also, post-training administration of the drugs was performed with the volume of 0.6 μl/rat (0.3 μl/side). Based on our findings, post-training bilateral intra-PL microinjection of ACPA (0.1 and 0.5 µg/rat) decreased, whereas RS67333 (0.5 μg/rat) increased IA memory consolidation. Meanwhile, post-training bilateral intra-PL administration of RS23597-190 (0.005, 0.01, 0.1 and 0.5 μg/rat) did not alter memory consolidation. Moreover, intra-PL microinfusion of RS67333 (0.005 μg/rat) plus the lower (0.001 µg/rat) or the higher (0.1 µg/rat) dose of ACPA potentiated or restored the memory consolidation impairment induced by ACPA, respectively. While, post-training administration of RS23597-190 (0.5 μg/rat) plus the higher dose of ACPA (0.1 μg/rat) potentiated the ACPA response. However,  none of the above interventions did not affect locomotor activity. In conclusion, our results suggest that the PL 5-HT4 receptors are involved in the modulation of ACPA-induced amnesia.

Biography:

Victor Manolov has completed his PhD from Medical University in Sofia, Bulgaria. He is working as Assist. Prof. at Department of Clinical laboratory and clinical immunology at the same University. He has interests in iron metabolism, gynecology, neurology, endocrinology and pediatrics. He has published more than 25 papers in reputed journals and participated in more than 60 National and International meetings in different medicine fields.

Abstract:

Alzheimer’s disease (AD), Parkinson’s disease (PD) and Amyotrophic Lateral Sclerosis (ALS) are part of neurodegenerative diseases. Their development is slow, progressive and most common is seen in elderly patients. Hepcidin leads to iron deposition in neuronal structures as a result from oxidative stress. We tried to evaluate serum hepcidin levels in neurodegenerative diseases and search for connection to disturbed iron homeostasis. 23 patients with AD, 17 cases with PD and 13 with ALS were included; 24 males (45.3%). They were clinically and neurologically reviewed, EMG; IMT and ABI were measured. They were evaluated for routine biochemical parameters, and additional serum hepcidin were quantified. AAS, nephelometric, ELISA and statistical methods were used during analyzes and obtained results interpretation. All results were compared to age and gender matched healthy controls. We found statistically significant elevated serum hepcidin in patients with neurodegenerative diseases (AD: 47.9 ± 3.1 µg/L; PD: 49.8 ± 5.1 µg/L; ALS: 53.8 ± 4.9 µg/L) compared to healthy controls (19.9 ± 4.1 µg/L); P<0.001. Serum hepcidin correlates negatively to glutathione peroxidase and superoxide dismutase changes in evaluated neurodegenerative diseases patients (0.9

Biography:

Nancy Brassard is a professor-researcher at the ENA University of Quebec teaching psychology, work, and mental health. Recently, completed superior studies in neuroscience to understand better the brain, its functions and those pathologies related like depression and FTD.  Scientist with a strong family history of FTD. 

Abstract:

At the beginning of Nancy Brassard mother’s disease, felt that I have to do something to help or to stop that! I began at this time to work intensively on what I am calling: The Quest! I asked my family members to participate with my mother and me at the study. I collected a lot of datas, made interviews and I built the whole family symptoms and history. This “Quest” led me to the Aging and memory center in May 2016, as a visiting scholar and to contribute slightly in the laboratory activities of Dr. Rankin. In last August, I had the honor of being invited by Dr. Bruce Miller to speak at the opening conference of Tau consortium in Denver. The title for my presentation was: Patient advocacy: A family story. At that time, I perceived the urgent need to help and support people dealing with a familial reality of FTD. This is unique!

I have initiated the past two years, studying in medicine and neuroscience, to better understand degenerative brain diseases especially, the stages, the onset of symptoms and the link with other variables such as, personality traits or lifestyle. I know that I can contribute to your event in many ways. First, I am teaching at the University since 12 years. I can contribute by my undeniable teaching skills, my openness and my strong ability to work in team. I have a strong research expertise and my scientific research skills are recognized by the scientific community. Second, being myself at risk of a brain disease, and as the President-founder of a non-profit Society, I am a great “Ambassador” to contribute with the researchers in the field in participating to their projects or to answer their questions, and share with them the importance of finding a cure for the families. I am hopeful, in a positive mind and I feel like if I have a mission. As a researcher, and especially as a daughter, and most of all, as a mother, I am in a Quest! Willing to participate or collaborate to find a cure or treatments and help people to deal with the disease and conciliate, understand and live with those realities. I want to be an example to show them that it is possible. I did it, I am doing it and I will continue to pursuit this Quest with passion, dedication and compassion.

Biography:

Abstract:

Bangladesh is a small densely populated country facing problems of communicable and non-communicable diseases. By the enormous efforts of Government and non-Government agencies with the help of world health organization (WHO) communicable diseases have been kept under control or some of them are eradicated; however, at the same time there is emergence of no ncommunicable diseases (NCD) like diabetes mellitus, hypertension, is chaemic heart disease, cancer and stroke which are partly due to increase of expectancy of life as well as sedentary life style faulty food habit and others. All the important NCDs are prevalent in the country of which stroke demands spinal attention due to increase morbidity and mortality. Stroke is one of the commonest neurological diseases that affect a significant number of the population in Bangladesh. Furthermore, there are other neurological diseases like head injury, brain tumor, epilepsy, meningitis, encephalitis and many more. Therefore a large number of patients admitted everyday into the hospital for treatment purposes. However, due to limited facilities of intensive care unit (ICU), hospital bed, and interventional neurology in the hospital these cause a great burden to the health sector of Bangladesh. In addition to that lack of advance technologies cause delayed diagnosis leading to influence the patients to go to abroad for better treatment. Therefore huge amount of foreign currencies are drained every year. Keeping all these things in mind the member of the society of Neurosciences have decided to establish National Institute of Neurosciences (NINS) in Bangladesh with the vision of making this Institute as the centre of excellence not only in this country but also for others. Ultimately the present NINS is the outcome of this effort. Currently this is the only referral tertiary care Neurology hospital in Bangladesh dealing with neurological as well as neurosurgical diseases. The current objective of NINS is to provide treatment to different neurological and neurosurgical cases in this country and to do the scientific research works as well as to collaborate with the other parallel institutes in abroad. It is a matter of pride that the institute has started functioning from September 2012 with OPD, IPD, emergency, ICU services as well as well equipped operation theater (OT) facilities. There are more than 15 departments related to neurological and neurosurgical diseases with more than 150 faculty members. Neurophysiology and interventional neurology are the two newly established departments which have been established first time ever in Bangladesh at public health sector. The NINS should be the centre of excellence in the country in near future where there should be the provision for one step services for the neurological cases. By this time the Institute has got its working life with the presence of 800 to 1000 patients in OPD everyday and 8 to 10 minor to major operation and the work in the Para clinical departments.

Biography:

Dr. Shang-Hsun Yang is the Associate Professor in Department of Physiology, at National Cheng Kung University, Tainan, Taiwan. He received his B.Sc. degree at National Chung Hsing University in 1998, M.Sc. degree at National Taiwan University in 2000 and Ph.D. degree at Emory University, USA, in 2008. He has developed his own research career at NCKU since 2009. His research interests focus on the regulation of microRNAs on HD, and tries to understand the regulatory mechanisms and potentially therapeutic directions for this neurodegenerative disease. Additionally, he also attempts to expand his research fields to other neurodegenerative diseases, and wishes to demonstrate the relationship between specific microRNAs and neurodegenerative diseases

Abstract:

Huntington’s disease (HD) is a genetic disease, and caused by a mutation in Huntingtin gene, leading to neuropathological symptoms. To date, there is no effective medicine for HD. Based on previous studies, transcriptional regulation is impaired during the progression of HD, and regulation of microRNA(miRNA) is one of affected mechanisms. Since HD leads to dysfunction of gene regulation and one miRNA could target to multiple pathways, it suggests miRNA could be one potential treatment for HD. In my laboratory, we identified one potential miRNA, miR-196a, from HD transgenic monkeys, and found the neuroprotective effects of miR-196a on HD in cell, transgenic mouse and HD patient-derived induced pluripotent stem cell models. miR-196a could not only improve molecular, neuropathological and behavioral phenotypes in transgenic mouse models, but also suppress pathological aggregates in neurons derived from HD patients. Furthermore, we also investigate molecular mechanisms of miR-196a, and show miR-196a could enhance cellular morphology, intracellular transport, synaptic plasticity, neuronal activity, learning and memory both in vitro and in vivo. In addition, miR-196a could work through binding to 3’ untranslated region of RAN binding protein 10 (RANBP10) to suppress the protein expression, further enhancing the assembly of β-tubulin. Most importantly, overexpression of RANBP10 led to worse neuronal morphology and severer pathological phenotypes in the HD transgenic mouse model, suggesting that miR-196a enhances neuronal morphology through suppressing RANBP10 to provide neuroprotection in HD. These results suggest the important role of miR-196a on HD, and might provide a new insight of therapeutical strategy for HD

Biography:

Asst professor Eyleen Goh is a senior research scientist at the National Neuroscience Institute and an assistant professor with the Duke-NUS Medical School in Singapore. Her research laboratory aims to understand the fundamentals of brain development and functions, and to search for possible intervention strategies for neurodevelopmental and neurodengenerative disorders. Besides the usual pharmaceutical approach, they are also exploring nutraceutical approach for the treatment of these brain disorders. Using cell cultures, animal models and human patient-derived cells, the lab is investigating the effects of micronutrients on neuronal development, circuitry and cognitive functions, to understand how micronutrients or the transport of these micronutrients affect brain functions and to determine if micronutrients can be used as treatment for neurological disorders.

Abstract:

Rett syndrome (RTT) is a postnatal neurodevelopmental disorder that primarily affects girls, with 95% of RTT cases resulting from mutations in the methyl-CpG-binding protein 2 (MECP2) gene. To model RTT in vitro, a short hairpin RNA was used to knockdown the expression of MeCP2 in primary neurons.  Abnormalities in the cholinergic system have been shown to be associated with the disorder. We found choline supplementation to MeCP2-knockdown neurons increased their soma sizes, and the complexity of their dendritic arbors. Through the use of specific inhibitors targeting each of the known physiological pathways of choline, synthesis of phosphatidylcholine from choline was found to be the most important pathway in bringing about the changes seen in choline-supplemented MeCP2-knockdown neurons. Rescue of the morphological defects could lead to enhanced neurotransmission, as suggested by an observed trend of increased expression of selected synaptic proteins in choline-supplemented cells, and differences in dendritic spine density and shape between wild type and Mecp2-knockout mice, with choline or vehicle supplementation. In addition, choline supplementation to cultured hippocampal neurons restored mini excitatory postsynaptic current frequencies in MeCP2-knockdown cells to control levels, while the amplitude was unchanged. Choline treatment to MeCP2-knockout mice also rescued deficits in motor coordination, anxiety-like behaviour, and social interaction. Taken together, these data reveal a role of choline in modulating neuronal plasticity, possibly leading to behavioural changes, and hence, a potential for using choline to treat RTT.

Biography:

Dr.  Ashutosh Kumar is the coordinator for the Etiologically Elusive Disorders Research Network (EEDRN), New Delhi, India: a research group which organizes collaborative research on difficult to treat human diseases for which etiology is exactly not known. His research group has recently made many noticeable publications in international peer reviewed journals. He is a medical post graduate from All India Institute of Medical Sciences (AIIMS), New Delhi, has been faculty in Anatomy at Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Karaikal, Pondicherry. He is currently working as the research associate at Laboratory of Molecular and Cell Biology, Department of Anatomy, AIIMS, New Delhi.

Abstract:

The etiomechanism of psychiatric disorders is still little understood. Optogenetically induced changes in neural networks and consequent change of behaviour in transgenic animals has provided a novel opportunity to develop animal models of various psychiatric disorders. We hereby propose zebrafish as a model organism based on the premise of its intricate analogy with mammalian brain. The habenula is an evolutionarily conserved bilateral structure located at the interface of diencephalon, basal nuclei and brainstem working as a gateway between cortical-subcortical and brainstem structures. Multiple studies have suggested master role of habenula in control of adaptive behaviour through regulation of brainstem aminergic nuclei. It is thought to function as a switchboard for regulating emotional behaviour in conditions facing survival challenges. The dysregulation of the emotional behaviour has been at the base of psychiatric disorders, and a functional manipulation of specific habenular nuclei using optogenetics combined with incremental levels of stress challenge may prove to be a basic model for the genesis of psychiatric disorders. Conversely, reversing the manipulation, scaling down stress levels, and providing enriched environment may ease psychiatric symptoms. The present article has proposed a hypothesis on the development of a basic zebrafish model for the psychiatric disorders based on this concept. Such a model may be of great help in understanding the common mechanism involved in genesis, progression of various psychiatric disorders. The article has also elaborated on the operational mechanisms and validity of the methodology, and has suggested an experimental design for the proposed study model.

Biography:

Chun-Wei Hsu is doing her Ph.D. in Psychology at University of Plymouth since April 2014. She went to undergraduate school at National Taiwan University, and double majored in life science and psychology within four years (Sep. 2007 – Jun. 2011). Later, she completed a master’s degree in Cognitive Neuroscience and Human Neuroimaging at University of Sheffield (Se. 2012 – Aug. 2013). Currently, her Ph.D. project is to explore the cognitive mechanisms underlying deception through creativity and neuroscience. Chun-Wei is interested in how people conduct high-level cognition in complex social interaction and how people evaluate expect the pay-offs and take action during the decision-making process. Ideal interaction requires people to simulate others' perspectives and shape their behaviors, which is of great interest to her. Human neuroimaging methods with fMRI or EEG are the approach she wants to use to answer my research questions

Abstract:

Concealed information paradigms (CITs) have been developed to determine if an individual is familiar with a certain piece of information such as a crime-related item. The main logic of CITs is that recognition of an item of interest (probe) will generate a differential response, compared to suitable control items (irrelevants), that can be detected by monitoring behavioral, psychophysiological, or neural variables.

An important issue is an extent to which countermeasures used by suspects can reduce the accuracy of the CIT. Recent work has focused on neural variables measured with functional magnetic resonance imaging (fMRI) because at first sight, such variables may seem more resistant to countermeasures than more peripheral variables. Previous work has shown that hybrid physical and mental countermeasures can decrease the accuracy of fMRI-based CITs, but questions remain as to whether purely mental countermeasures can do so as well. Existing evidence shows that attentional and memory strategies can decrease the accuracy with which one can use fMRI to detect successful recognition in standard face recognition tasks.

The aim of this fMRI study was to determine if such mental countermeasures are effective also with standard CITs. Participants (N=20) were tested under three conditions: no knowledge, concealed knowledge, and countermeasures. Results based on regions of interest defined in previous CIT studies showed that the area under the curve (AUC) for discriminating no knowledge and concealed knowledge cases with multi-voxel pattern analyses was 0.86 without countermeasures. Critically, memory and attentional countermeasures significantly reduced the AUC to 0.74.

These results indicate that purely mental countermeasures can reduce the accuracy of fMRI-based CITs, even without extensive training of participants. 

Biography:

Amira Elaalem is 27 years old female, completed her master degree in Neurology physiotherapy at Alneelain University (Sudan).  Studied physiotherapy BSC at Alneelain University Faculty of Medicine and health science, and now studying in my last year in MBBS program. She finished Diploma degree at research methodology and ethics held at Alneelain University and collaboration with Maryland University. Her research publication is under process.

Abstract:

Bells palsy is the idiopathic seventh cranial nerve palsy. It is the most common cause of abrupt onset of unilateral facial weakness. The natural history of Bell’s palsy is encouraging for most of the patients since total recovery of facial function is expected, nevertheless additional long term poor outcomes occur in minority of them and can be devastating. Currently, no cause for Bell’s palsy has been identified in the literature, but in Sudan there were very few information can be retrieved.

Hence the overall objective of the study was to assess the potential relative risk factors of Bell’s palsy in Sudanese patients. 

Methodology

This is analytic case control multicenter based study. Conducted in Khartoum state physiotherapy centers (three in hospital and seven in private sectors) July - November 2016. The sample size was 70 cases of Bell’s palsy and 140 controls from the same sample area. The cases that fulfilled the inclusion criteria were collected by a method of total coverage during the working hours. Well constructed questionnaires were filled during the interview by a trained physiotherapist. The collected data was then analyzed using SPSS software program, version 20.

Results

The result showed the statistically significant factors (p value < 0.05) are: recurrence of Bell’s palsy ten times more in affected patients, the hereditary factor 2.5 times more in affected patients. In contrast to the other factors were non statistical significance (p value > 0.05) are: recent vaccination, pregnancy, diabetes, hypertension, chronic diseases, immunosuppressive drugs, smoking and alcohol and.

Conclusion

The study concluded that, statistical significant factors are frequency of recurrence of Bell’s palsy, genetic susceptibility. The rest of risk factors were statistical non significant.

 We recommend more studies deserve to be done to determine the type of inheritance in Sudan and study the cause of recurrence

Biography:

Arunkumar Prasad is the last year student in Taishan Medical University, China. He is the President of the Student Oragnisation in the field of Academics and other activities in TSMU. He was one of the speaker at the Euro Brain Injury 2017 held in London, UK. He is currently working as a young researcher and studying under his Professor Baoliang Sun (Neurologist, PhD, Dean of TSMU).

Abstract:

Recent studies suggest that CNS lymphatic drainage pathway to extracranial lymph compartments may play an important role in the removal of substances in the brain and cerebrospinal fluid (CSF). After the onset of subarachnoid hemorrhage (SAH), large amount of macromolecular substances, such as cellular lysates, proteins, peptides, were accumulated in the brain tissue and CSF, which contribute to cerebral vasospasm and cerebral injury. The present experiment was carried out to investigate the possible role of cerebral lymphatic drainage pathway in the development of cerebral vasospasm and related cerebral injury and the influence of Ginkgo biloba extract. Wistar rats were used in the experiment and animals were divided into different groups. SAH models were replicated by double cisternal injection of autologous arterial hemolysate. In some animals the main cerebral lymphatic drainage way out being blocked (cerebral lymphatic blockade, CLB). Two different constituents, Ginkgolides and Ginkgo flavone, were given as interventions. It was found that SAH reduced the drainage of Evans blue-labeled albumin (EBA) from the brain to the olfactory bulbs, cervical lymph nodes and abdominal paraaortic lymph nodes. A kinetic analysis of 125I-labeled human serum albumin (125I-HSA), a cerebrospinal fluid (CSF) tracer, showed that the clearance rate of macromolecules in the CSF was significantly reduced after SAH. Furthermore, SAH reduced the diameters of basilar artery (BA) and increased thickness of BA. Prominent cerebral injury was found after induction of SAH. The spasm of BA and cerebral injury were partially antagonized by Ginkgolides and Ginkgo flavone. It was concluded that cerebral lymphatic drainage pathway exerts intrinsic protective effects against cerebral vasospasm and cerebral injury by removal of macromolecular substances in the brain and subarachnoid spaces. Ginkgolides and Ginkgo flavone may alleviate the exacerbated cerebral vasospasm and cerebral injury following SAH by CLB.

Biography:

Yusuf Issa Olakunle is a PhD student in Taiwan International Graduate Program (TIGP) Academia Sinica of the Neuroscience, at National Cheng Kung University (NCKU). He obtained his B.Sc. degree in Physiology from Ahmadu Bello University, Zaria, Nigeria, in 2010, and M.S.c degree in Physiology from the University of Ibadan, Nigeria, in 2014. He currently conducts his research works in Dr. Yang’s laboratory in the Department of Physiology, NCKU, and demonstrates on the therapeutic roles of FGF9 and miR-196a in Huntington’s disease (HD). 

Abstract:

Statement of Problem: Huntington’s disease (HD) is a heritable neurodegenerative disorder characterized by selective and progressive damage of medium spiny neurons in the striatum, and there is no cure for HD to date. A type of fibroblast growth factor (FGF), FGF9, has been reported to play prosurvival roles, in other neurodegenerative diseases, such as Parkinson’s disease and Alzheimer’s disease. With many similarities in the cellular and pathological mechanisms that eventually cause cell death in neurodegenerative diseases, we hypothesize that FGF9 might provide neuroprotective functions in HD. Methods and Findings: Here, we used STHdh^Q7/Q7 (WT) and STHdh^Q111/Q111 (HD) striatal knock-in cell lines as our models, and examined the neuroprotective effects of FGF9 on HD. Employing MTT and PI staining assays to determine cell proliferation and survival respectively, we found that FGF9 enhanced cell proliferation and also increased cell survival under a starvation stress condition. In addition, we observed that FGF9 significantly upregulated FGF signalling through ERK1/2, Akt, JNK, and mTOR pathways, and increased neurotrophic factor (GDNF) and anti-apoptotic BcL-xL proteins in HD cells. Especially, ERK pathway plays a critical role in the effects of FGF9 on cell survival and GDNF regulation. Conclusion and Significance: These results not only show the neuroprotective effects of FGF9, but also clarify the critical mechanisms in HD cells, further providing therapeutic potential of FGF9 in HD.