9^th Global Summit on
Neuroscience and Neuroimmunology

Biography:

Dr. Veronika Neubrand possesses a Biology degree from the University of Heidelberg and a PhD from the European Molecular Biology Laboratory (EMBL) and the University of Heidelberg, Germany. Currently she holds a substitute professorship at the department of Cell Biology at the University of Granada, Spain.

In 2009 at the IPBLN-CSIC, Granada, Spain, she started to study the cell biology of microglia, the immune cells of the brain, which play an essential role in neuroinflammation, an important hallmark of neurodegenerative diseases, such as Alzheimer´s and Parkinson´s. In 2014, she was awarded a research grant by the Michael J Fox Foundation, USA. As principle investigator of this grant she identified molecules involved in the generation of CNS-supporting microglia, which represent drug targets for the diseases mentioned above. From 2005 to 2009, Veronika investigated the molecular mechanisms of axonal and dendritic growth in neurons at the Cancer Research UK London Research Institute.

Abstract:

Over-activated microglia, the resident immune cells of the brain, play a central role during neuroinflammation, leading to neuronal cell death and neurodegeneration, for example in Alzheimer´s and Parkinson´s disease. Reversion of these over-activated microglia to a neuroprotective phenotype could regenerate a healthy Central Nervous System (CNS)-supporting microglial environment. Our aim was to identify a dataset of intracellular molecules in primary microglia that play a role in the transition of a neurotoxic phenotype to a ramified, neuroprotective one. To do this, we exploited the anti-inflammatory and neuroprotective properties of conditioned medium of adipose-derived mesenchymal stem cells (CM) as a tool to generate the neuroprotective phenotype of microglia in vitro, and we set up a microscopy-based siRNA screen to identify its hits by cell morphology.

We assayed an siRNA array targeting more than 150 genes that codify proteins of cytoskeleton and inflammatory pathways in microglia. From them, siRNA-downregulation of more than 40 genes significantly inhibited the CM-induced transition from a neurotoxic to a neuroprotective microglia phenotype, and 50 siRNA-downregulated genes had the opposite effect. As a proof-of-concept, ten of these targets were validated with individual siRNAs and by downregulation of protein expression. This validation step resulted to be essential, because three of the potential targets were false positives. The seven validated targets were assayed in functional screens that revealed that the atypical RhoGTPase RhoE/Rnd3 is necessary for BDNF expression and plays an essential role in controlling microglial migration.

Besides the identification of RhoE/Rnd3 as a novel inducer of a neuroprotective phenotype in microglia, we propose a list of potential targets to be further confirmed with selective activators or inhibitors.

Biography:

 Einstein's area of specialization is neuro-immunology and neuro-regeneration in neurodegenerative diseases, specifically on animal models of human Multiple Sclerosis (MS). Her major studies concern on the neurobiology of neural stem cells and cell therapy in neurodegenerative diseases. Her work published in 2003 was the first to show that transplanted neural stem cells have anti-inflammatory effects on the rodent brain. This finding was a breakthrough for further research of her group, as well as other research groups around the world. Her current research focuses mainly on neuro-immunological, neuro-protective and neuro-regenerative effects of exercise training on neurodegenerative diseases, particularly on experimental autoimmune encephalomyelitis (EAE) the animal model of MS. The studies involve animal training, clinical evaluations, histopathological analyses, cell cultures and molecular biology techniques. 

Abstract:

 Exercise training (ET) has beneficial effects on multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE). However, the intensity-dependent effects of ET on the systemic immune system in EAE remain undefined. Objective: (1) To compare the systemic immune-modulatory effects of moderate vs. high intensity ET protocols in EAE; (2) To investigate whether ET affects autoimmunity selectively, or causes general immunosuppression. Methods: Healthy mice were subjected to moderate or high intensity treadmill running programs. Proteolipid protein (PLP) -induced transfer EAE was utilized to examine ET effects specifically on the systemic immune system. To examine effects of ET on systemic autoimmunity, lymph-node (LN)-T cells from trained- vs. sedentary donor mice were transferred to naïve recipients and EAE severity was assessed. LN-T cells derived from donor trained vs. sedentary PLP-immunized mice were analyzed in vitro for proliferation assays and cytokine and chemokine receptor genes expression. T cell-dependent immune responses of trained- vs. sedentary mice to the non-autoantigen ovalbumin and susceptibility to Escherichia coli - induced acute peritonitis were examined.  Results: High intensity training in donor mice induced stronger inhibitory effect than moderate intensity training on disease development and PLP-reactivity of LN- T cells derived from PLPimmunized mice. High intensity training also inhibited LN- T cell proliferation in response to ovalbumin immunization. E-coli bacteria counts and dissemination were similar in trained and sedentary mice. Conclusion: High intensity training possesses superior modulatory effects on autoimmunity in EAE, while also inhibiting T cell responses to ovalbumin, but sustains immune defenses against E-coli bacteria. 

Biography:

Samuel Perez is currently working as an assistant professor in Washington Adventist University, Maryland. He acheived his PH.D in the area of Neurophysiology/Neuroimmunology at Loma Linda University School of Medicine, California. Sam D Perez obtained the degree of master’s in Molecular Physiology at Loma Linda University. His scientific research interest includes : Study the effects of neuroprotective micronutrients on learning and memory function in animal models using molecular biology tools and animal models to understand neuroimmune mechanisms of cell protection and many more...

Abstract:

Senescence of innate and adaptive responses and low-grade inflammation(inflammaging) hallmarks normal aging, which increases vulnerability to infectious diseases, autoimmunity and cancer. In normal aging, sympathetic dysregulation contributes to the dysregulation of innate and adaptive immunity and inflammaging. Sympathetic innervation of immune cells in secondary immune organs regulates immune responses. Different profiles of sympathetic signaling during aging may bring about different effects on neurotransmission in immune cells that may lead to immunity variation in senescence. We investigated whether increased sympathetic nerve activity (SNA) in the aging spleen contributes to agerelated sympathetic neuropathy and altered neurotransmission in splenic lymphocytes of two strain of rats of strikingly different sympathetic activation and behavior profiles. To answer this question, we injected 15 month-old rats, of either strain, 0, 0.5 or 1.5 μg/kg/day rilmenidine intraperitoneally, for 90 days to lower sympathetic tone. Untreated young and age-matched rats controlled for effects of age.  We found that in Fischer 344 (F344) rats, an age-related increase in sympathetic tone and sympathetic dysfunction in beta-adrenergic receptor (AR) signaling of splenic lymphocytes contribute to immune senescence. In the much longer-lived Brown-Norway (BN) rats, we observed that elevated SNA in the aging BN rat spleen does not contribute significantly to sympathetic neuropathy or the aging-induced impairment of canonical β-AR signal transduction. Despite the rilmenidine-induced increase in β-AR expression, splenocyte c-AMP production was comparable with age-matched controls, thus dampening nerve activity had no effect on receptor coupling to adenylate cyclase. Understanding how aging differentially affects neuroimmune regulation in healthy aging rodent of different strain models can help us formulate strategies to improve health in aging populations that are most vulnerable to immunosenescence and lowgrade systemic inflammation.   

Biography:

Giovanni Antioco Putzu is a Medical Doctor since 1992, with specialization in Paediatric Neurology. He achived his PhD in 1996. During PHD studies, He was a Research Fellow in Hammersmith Hospital of London, UK in 1992, then He moved to Marseille (France)  to work at INSERM (Genetics) and in Neurophathology. The Author has published more than 15 papers in the field of Neuromuscular Disorders.

Abstract:

GBS is an auto-immune life-threatening inflammatory polineuropathy that may produce severe functional disability. Vaccines, viral, fungine or bacterial infections may trigger the disease. On the basis of neuropathological and neurophysiological findings, GBS is classified in demyelinating and axonal forms. In both features, functional disability is directly correlated to axonal loss. Involvement of amyelinic axons is responsible for autonomic disturbances, which, along with bulbar spread of the disease, represent a potential cause of death in GBS. A consistent number of patients both in the early or recovery phases may complain of neuropathic pain that requires an adequate treatment. Immunological aspect of the disease, i.e auto-antibodies directed against GM1 and recently to contactin-associated protein 1 (Caspr) of the paranodal region of myelinated nerves, have already been investigated. We have demonstrated that TNF-alpha was immunolocalized in both myelinated and unmyelinated axons the sural nerve of GBS patients. We concluded that this substance may be directly responsible for axonal loss( G.A. Putzu et al, J. Neurol Sci, 2000).

Interferon-gamma, which is a stimulator of IL28A was also easily detected in the sural nerve of GBS patients. The role of adhesion molecules like ICAM in the immune process of GBS will be also discussed. The therapeutic approach of GBS is aimed to avoid death in the acute phase (respiratory failure in Landry paralysis, cardiac rhythm anomalies in disautonomia). The efficacy of plasmapheris and intravenous immunoglobulins in the treatment of GBS is nowadays clearly demostrated. The next frontier is the theoretical possibility to use monoclonal antibodies (i.e, anti-INF-gamma) as a therapeutic tool in GBS.

We also reviewed the literature on GBS-like conditions that may clinically mimick GBS.

Biography:

Abstract:

Biography:

Dedicated RPT offering 4 years of experience in physical therapy field. A history of exemplary ratings on performance reviews; bilingual fluency (English and Arabic) and solid credentials that includes Egyptian licensure, B.Sc degree in physical therapy and Master degree with GPA 2.63. Background includes work with neurologic, orthopedic and pediatric patients. Well-versed in a broad range of PT programs, treatments and modalities restoring function and mitigating disability for diseased and injured patients. Excellent interpersonal/communication skills and proficiency in patient assessment, time management and therapy program design/execution. Enthusiastic team player deeply committed to delivering quality care and achieving superior patient outcomes as a member of a multidisciplinary case-management team. 

Abstract:

Post stroke dysphagia (PSD) can decrease the quality of life, increase the risk of medical complications and mortality. So it is a great concern for patients and a tough problem for clinicians. Purpose: The current study was conducted to investigate the effect of adding TENS to the conventional therapy of treating PSD. Methods: Thirty patients complaint from post stroke dysphagia were participated in this study, their ages were ranged from 45 to 85 years. They were randomly divided into two equal groups. Group (A): Received 3 weeks of treatment with Transcutaneous Electrical Nerve Stimulation (TENS), frequency 80 HZ, pulse duration of   300 μsec, intensity according to the patient’s tolerance ranging from 2.5 to 25 mA, duration of treatment 30 min three times/week in addition to the conventional therapy. While Group (B): Received 3 weeks of treatment with conventional therapy and placebo TENS, duration of treatment 30 min three times/ week. Results: Both treatment protocols are effective, minimally invasive option for treatment of patients complaining of post stroke dysphagia, both groups produced subjective improvement and there is a significant increase in both The Functional Oral Intake Scale (FOIS) and The Mann Assessment of Swallowing Ability (MASA) of group A compared with that of group B post treatment. Conclusion: There was significant increase in the MASA of group A compared with that of group B post treatment. Moreover, there was a significant increase in the median values of FOIS of group A post treatment compared with that of group B

Biography:

Abstract:

Impairment in cognitive functioning and motor activity are commonly encountered in patients affected by MS. The aim of this study was to investigate the impact of induced depression on cuprizone mouse model of demyelination and the effectiveness of enhanced environment (EE) as a method of intervention. C57BL/6 male mice were divided into cuprizone only (Cup-O), cuprizone undergoing depression (Cup-Dep), cuprizone housed in EE (Cup-EE), cuprizone housed in EE and undergoing depression (Cup-ED) and control groups (9 to 10 per group). Depression was induced by repeated open-space forced swim. Neurobehavioral tests were conducted after a six-week period of 0.2% cuprizone-enriched diet. Cup-EE performed significantly better in fields of cognition and motor functioning when compared to Cup-O as evident by Morris water maze (p<0.001) and rotarod (p<0.05) results. Contrariwise, Cup-Dep showed a significantly declined performance in Morris water maze (p<0.001) and rotarod (p<0.05) in comparison to Cup-O. Cup-ED had comparable results to Cup-O indicating reversal of induced depression effects. Open field test results failed to show an anxiety-like behavior in cuprizone mouse model. It is concluded that environmental enhancement can improve MS-associated cognitive and motor deficits. Insights gained from these results facilitate the exploration of non-medical modes of intervention as an emerging adjuvant therapy in MS.

Biography:

Arturo Solis-Herrera is specialized in ophthalmology at the UNAM, accrediting various courses at the Hospital Conde Valenciana and the National Institute of Neurology. In the year 1982, Dr. Solís Herrera began working in the state of Aguascalientes, where worked at the Autonomous University of Aguascalientes and the Mexican Institute of Social Security. The private practice of ophthalmology of Dr. Solis Herrera, to start in the year of 1990, observational, descriptive research; about the morphological changes in the tiny blood vessels that come in and out of the optic nerve and its possible correlation with the three leading causes of blindness in Mexico and the world: Glaucoma, diabetes, and macular degeneration. This study culminated twelve years later and included retina photographs of six thousand patients; with the discovery of the unsuspected intrinsic property of melanin to transform visible light into chemical energy, through the dissociation of the water molecule, such as chlorophyll, in plants. Also, already dedicated to private practice and research of melanin, Dr. Solis Herrera obtained the degree of master’s in medical sciences at the Autonomous University of Aguascalientes and later the doctorate in Pharmacology (toxicology) in the University of Guadalajara.

Dr. Solis Herrera is founding director of the Center for Studies of Human photosynthesis®, S.C. in Aguascalientes; Mexico. Unique institution of its kind in Mexico and the world. It should be mentioned that Dr. Arturo Solís Herrera conducted the research in his private office, with his own means, financing the project with his daily work. 

Abstract:

Statement of the Problem: Glucose is considered to this day as the source of energy par excellence of the CNS. Biology and medicine are completely based on this dogma. On the other hand, the neuromelanin was considered a waste of the metabolism of norepinephrine in the CNS. Therefore, the pathophysiology of CNS diseases was studied thinking that glucose was able to provide the building blocks of organic molecules that conforms us, and at the same time was able to provide the energy that its own metabolism requires. But trying to explain the biochemical basis of the functioning of the body based on the dual function of glucose (mass and energy) has led us to travel on unnecessarily complex roads that are theoretical in 95%. What is the result of the scarce therapeutic results in neurodegenerative diseases such as AD, PD, Huntington, coma, PTSD; etc.  The purpose of this study is to describe the notorious difference between previous biology and the new neurobiology based in glucose as source of biomass and neuromelanin as source of energy. Methodology & Theoretical Orientation: The division between mass and energy allows a different conceptualization in the functioning of the CNS. The discovery of the unsuspected neuromelanin ability to transform the light into chemical energy through the dissociation of the water molecule, like chlorophyll into plants, shatters the sacrosanct role of glucose as a source of energy. Our finding about the ability of neuromelanin to dissociate the water molecule occurred during an observational, descriptive study of the three main causes of blindness (Glaucoma, diabetes, and macular degeneration) and its relationship with morphology of the tiny optic nerve vessels. The protocol lasted twelve years, and 6000 patients were included.  Findings: Glucose is sources of structured carbon chains in a surprisingly accurate way. That way our body gets C, H, and oxygen. Glucose is the universal precursor of 99% of the body's organic matter, but it cannot provide the energy that its own    metabolism requires. Conclusion & Significance: The discovery of the unsuspected bioenergetic role of Neuromelanin, opens a new era in Neuro sciences. It simplifies the metabolic pathways and facilitates the development of efficient therapeutic schemes in diseases considered incurable, such as AD, PD, Huntington, coma, PTSD, etcetera.

Biography:

Shabbir Saifuddin received post-graduate degree in Ophthalmology in 1987 from Mangalore University in India and has undergone clinical trainings at London  MOORFIELDS Eye Hospital)  and Munich  (University Eye Hospital ) and has 35 years of experience as an Ophthalmologist. He has published over 30 papers in journals and at various regional and international conferences. He is presently undergoing training for the MCh Ophthalmology degree.

Abstract:

As vision is the predominant sensory modality in the dreams of normally sighted people, it is reasonable to ask do blind individuals have visual dreams ? Blindness, particularly when it occurs early in life, is associated with reduced visual imagery and an increased incidence of sleep disturbances including more frequent nightmares. However, the sensory and emotional dream qualities of individuals with differing blindness etiologies remain poorly studied.The goal of the present study was to further assess the dream experiences of individuals with different times of blindness onset. We examined dream reports collected from 11 blind individuals who reported no light perception, and 11 age- and sex-matched normal-sighted controls. Of the blind individuals, 5 were born blind (congenital blind) and 6 had acquired blindness some time after birth (late blind). Dream content and themes were examined using daily dream questionnaires collected over a period of 30 days, as well as with the Inventory of Dreams: Experiences and Attitudes (IDEA) questionnaire and the Typical Dreams Questionnaire (TDQ). As expected, the incidence of visual dream elements was much lower in both groups of blind individuals, while other sensory modalities were more present. Further, congenitally blind individuals, but not late blind individuals, reported more nightmares. Although dream themes were generally similar between blind and normal-sighted individuals, as well as between the congenital and late blind groups, we noted some contents that were characteristic of the blind. Particularly, they reported a greater intensity of positive emotions in their dreams, as well as a more positive attitude towards the dreaming experience. Blindness not only results in the reduction of visual elements in dream content, but may alter their emotional quality, including a heightened frequency of nightmares among congenitally blind individuals.

Biography:

SUCHI is an experienced International Pre School Principal/Manager who picked up  Laughter exercises from many coaches around the world. She then designed ‘Laughter Therapy' which is being used  in many places such as hospitals and Senior Activity Centres. She provides individual and group therapy in educational and home settings.

Abstract:

Statement of the Problem: There is a lack of awareness about what happy hormones are ,how to use positive words to feel energetic and what can be done to get happy hormones. People tend to feel unhappy for multiple reasons and neuropathic pain adds on Stress levels of not only the patient but the caregivers as well. Being in pain leads to feeling depressed and anxious  in some cases.

Methodology & Theoretical Orientation: Review of Books and Research shows that getting a dosage of happy  hormones will not only ease slight  pain of the patient but  feeling happy will also have a positive impact on the recovery of the patient. Adopting  Laughter therapy and getting hormones which makes one feel good will help many to recover from Neuropathic pain  /Long term sadness caused by having  grief ,Anger or Resentment, Depression & Anxiety.

Findings: One needs to work on his/her energies using Laughter Therapy which is a  positive approach for not having Depression & Anxiety caused by Neuropathic pain . The therapy can be used as a Holistic way to  recovery. 

Conclusion & Significance: The Laughter therapy which includes ways to get the dosage of happy hormones promotes overcoming Depression & Anxiety caused by Neuropathic pain ,is  a fun way to manage pain.  Repeated sessions to be conducted to remind patients that  life while having pain or during the recovery should go beyond just seeking medical and counselling help and also include rebuilding Spiritual, Physical, Emotional, Relational and Mental health. The model has been put together from for testing in many settings including hospitals ,elderly homes and senior citizen centres.  This is not a research book or paper. It is just an effort to demystify the help available for Depression & Anxiety caused by pain. It is an attempt to motivate and encourage people to seek help and take a simple approach to remember and work on all aspects of their recovery. 

Biography:

Ranjana Arya completed Ph.D. in the field of Life Sciences from Jawaharlal Nehru University at the age of 29 years followed by post doctoral research experience at Harvard Medical School, Boston, USA and University of North Carolina, Chapel Hill, USA. I worked as Senior Research Scientist in pharmaceutical industry, Ranbaxy Research Laboratories, India for more than 3 years. Presently, I am Assistant Professor at School of Biotechnology, Jawaharlal Nehru University (JNU) since 2008. I have published 23 papers in reputed journals and guided 8 PhD research scholars as supervisor. I am also Assistant Director at University Grants Commission, Human Resource Development Centre, JNU, New Delhi.

Abstract:

Biological basis of pathogenesis of a large number of genetic disorders is not known, particularly for those diseases which affect the neuromuscular system. UDP-GlcNAc 2-epimerase /ManNAc kinase (GNE) is a bifunctional enzyme (N-terminal epimerase and C-terminal Kinase domain) that catalyzes rate limiting step in sialic acid biosynthesis. Homozygous misssense mutations in either epimerase or kinase domain of GNE leads to slowly progressive autosomal recessive genetic neuromuscular disorder, GNE Myopathy. These GNE related myopathies are characterized by hyposialylation of glycoproteins in muscle cells of patients and primary defect in either N or O-linked glycosylation. However, it appears from some recent experiments including those from our laboratory that mutant GNE may also affect targets that are not directly related to sialic acid biosynthesis. In particular cytoskeletal network, sarcomere organization and apoptotic signaling are likely to be altered in muscle cells. In absence of clear understanding of the pathomechanism, no treatment is currently available to cure the disease. Our laboratory focuses on deciphering alternate roles of GNE in regulating cell functions with an aim to identify more effective drug targets. We have established a HEK293 cell based assay system where pathologically relevant mutations of GNE are overexpressed alongwith GNE knockdown using shRNA. The system is validated by reduced sialic acid content of the cell and restoration of sialylation after supplementation with 5 mMsialic acid. Using this system, GNE has been shown to affect cell adhesion property via hyposialylation of β-1 integrin and altering G-actin and F-actin levels in GNE deficient cell lines. Mutation in GNE caused increased apoptosis via mitochondrial dysfunction that could be rescued by treatment with Insulin-like Growth Factor1 (IGF-1). Differential levels of ER resident Peroxiredoxin IV and upregulation of chaperones generate ER stress in absence of functional GNE. Thus drug molecules regulating chaperone function can modulate protein misfolding and prevent protein aggregation observed in GNE myopathy. Our study clearly provides a base for understanding pathomechanism of GNE myopathy and the opportunity of using cell-based assays for diagnostics as well as exploring pharmacological drug molecules.

Biography:

Dr Jeremy Isaacs is a consultant neurologist at St George’s Hospital and Kingston Hospital and Honorary Senior Lecturer at St George’s University of London.  He studied medicine at Cambridge and UCL.  His PhD was on the immunology of Creutzfeldt-Jakob disease (CJD).  His current research interests are in functional cognitive disorders, delirium and clinical trials in Alzheimer’s disease and vascular dementia.  Dr Isaacs was a member of the NICE 2018 dementia clinical guideline committee.  He is deputy clinical director of the NHS England (London) Dementia Clinical Network where he leads the London memory network, memory service audit and pathway streamlining programme.

Abstract:

Functional cognitive disorder (FCD) describes cognitive dysfunction in the absence of an organic cause. It is increasingly prevalent in memory clinics yet its key neuropsychological features have not been well studied.  We hypothesised that cognitive profiles in fibromyalgia (FM), chronic fatigue syndrome (CFS) and functional neurological disorders (FNDs) would provide a template for characterising FCD.

We conducted a systematic review of studies with cognition-related outcomes in FM, CFS and FND.  We selected 52 studies on FM, 95 on CFS and 39 on FND.  We found high rates of subjective cognitive symptoms, including forgetfulness, distractibility and word-finding difficulties, but inconsistent objective neuropsychological deficits.  Objective deficits were reported, including poor selective and divided attention, slow information processing and vulnerability to distraction.  In some studies, cognitive performance was inversely correlated with pain, exertion and fatigue. Performance validity testing demonstrated poor effort in only a minority of subjects.  Patients with CFS reported a heightened perception of effort in during testing.

The available data suggest that the cognitive profiles of FM, CFS and non-cognitive FND are similar to the proposed features of FCD, suggesting common mechanistic underpinnings.  Similar findings have been reported in patients with mild traumatic brain injury and whiplash.  We hypothesise that pain, fatigue and excessive interoceptive monitoring produce a decrease in externally directed attention.  This increases susceptibility to distraction and slows information processing, interfering with cognitive function, in particular multitasking.  Routine cognitive processes are experienced as unduly effortful.  This may reflect a switch from an automatic to a less efficient controlled or explicit cognitive mode, a mechanism that has also been proposed for impaired motor control in FND.  These experiences might then be overinterpreted due to memory perfectionism and heightened self-monitoring of cognitive performance.

We are currently testing several hypotheses generated by this review in a cohort of patients with FCD.

Biography:

Dr Serafeim Katsavos is a military neurologist and a PhD student of the National & Kapodistrian University of Athens (NKUA), examining the characteristics of familial Multiple Sclerosis in Greece. He gained expertise in Neuroimmunology as clinical fellow of the Dept of Clinical Neurosciences, in Addenbrooke’s CUH, and authored several scientific publications on Multiple Sclerosis pathophysiology and treatment.

Abstract:

Approximately 10% of Multiple Sclerosis (MS) patients have at least one relative who is also affected (familial MS/ fMS). Nevertheless, only scarce systematic attempts of further describing fMS have been done so far. In this study we examined the clinical, imaging and genetic profile traits of 123 fMS patients, compared to 275 sporadic cases (sMS). Methodology: Patients recruited underwent medical interview (demographic, clinical and family history data) and disability assessment, while their MRI-scans were analyzed for lesion distribution. HLA-DRB1 genotyping was performed for 53 non-related fMS and 52 sMS patients. Comparisons with HLA-DRB1 allelic frequencies, of a previously published sample of healthy controls (HC), were also performed. Findings: 47% of fMS cases had a 1^st degree relative affected, while the rest had a 2^nd or 3^rd degree relative. Only the former subgroup had significantly younger age at disease onset (AAO) compared to sMS cases (mean AAO 28.3 vs 31.2 years, p=0.042). AAO anticipation was noted in younger generation fMS patients (mean AAO 23.3 years vs 40.3 years in older generation, p=0.001). With regard to MRI findings, brainstem lesions were less frequent in fMS (50.8% vs 63.2% in sMS patients, p=0.039). 1^st degree relatives of fMS patients were more often diagnosed with Hashimoto’s (10.3% vs 3.3% in sMS relatives, p=0.02). HLA-DRB1*15 frequency was significantly increased in both sMS and fMS subgroups, compared to HC (34.6% & 32.1% vs 16.7% respectively, p=0.002), while HLA-DRB1*11 was significantly decreased only when comparing sMS with HC (30.8% vs 52%, p=0.002). Conclusions: fMS appears to differ from sMS in terms of lesion distribution. AAO observations could either be real or due to an ‘increased vigilance’ bias in fMS. Allelic distribution findings suggest that HLA polymorphisms are not the most important genetic risk factors for developing fMS, but rather their co-aggregation with multiple non-HLA genetic variations.

Biography:

Segundo Mesa Castillo. As Specialist in Neurology, he worked for 10 years in the Institute of Neurology of Havana, Cuba.  He has worked in Electron Microscopic Studies on Schizophrenia for 32 years. He was awarded with the International Price of the Stanley Foundation Award Program and for the Professional Committee to work as a fellowship position in the Laboratory of the Central Nervous System Studies, National Institute of Neurological Diseases and Stroke under Dr. Joseph Gibbs for a period of 6 months, National Institute of Health, Bethesda, Maryland, Washington D.C. USA, June 5, 1990. At present he is member of the Scientific Board of the Psychiatric Hospital of Havana and give lectures to residents in psychiatry.

Abstract:

There is increasing evidences that favor the prenatal beginning of schizophrenia. These evidences point toward intra-uterine environmental factors that act specifically during the second pregnancy trimester producing a direct damage of the brain of the fetus [1]. The current available technology doesn't allow observing what is happening at cellular level since the human brain is not exposed  to a direct analysis in that stage of the life in subjects at high risk of developing schizophrenia. Methods. In 1977 we began a direct electron microscopic research of the brain of fetuses at high risk from schizophrenic mothers in order to finding differences at cellular level in relation to controls. Results. In these studies we have observed within the nuclei of neurons the presence of complete and incomplete viral particles that reacted in positive form with antibodies to herpes simplex hominis type I [HSV1] virus, and mitochondria alterations [2]. Conclusion. The importance of these findings can have practical applications in the prevention of the illness keeping in mind its direct relation to the aetiology and physiopathology of schizophrenia. A study of the gametes or the amniotic fluid cells in women at risk of having a schizophrenic offspring is considered. Of being observed the same alterations that those observed previously in the cells of the brain of the studied foetuses, it would intend to these women in risk of having a schizophrenia descendant, previous information of the results, the voluntary medical interruption of the pregnancy or an early anti HSV1 viral treatment as preventive measure of the later development of the illness.

Biography:

Dr BK Bista, is one of the first neurologists of Nepal. He has been pioneering in field of neuroscience in Nepal and established the first neuroscience center of eastern Nepal. Through years the work of this neuroscience center has been recognized home and abroad. He shows keen interest in medical management and providing state of art services to this impoverished region of Nepal. Recently he  added the first stroke center of Nepal. He firmly believes in continuous updated education and its implementation in hospital practices.   

Abstract:

Stroke alters the cerebral autoregulation as a result blood pressure is elevated in most of the stroke patients. Different stroke types namely,  intracerebal hemorrhage, ischemic infarct and SAH (subarachnoid hemorrhage) each require different ranges of BP blood pressure optimization to maintain CPP and MAP. Inappropriate ranges of BP result as rebleed, infarct evolution and cerebral edema.  The stroke types require different MAP(mean arterial pressure), CPP (cerebral perfusion pressure), systolic blood pressure (SBP) and diastolic blood pressure (DBP) to maintain adequate cerebral perfusion. Blood pressure optimization is among one of the most important steps in neuroprotection. This systemic review presents the latest updates  in BP management in acute stroke. It also stipulates recommended ranges of CPP, MAP, ICP (Intracranial Pressure), SBP and DBP, for acute stroke management. Emphasis on, injectible antihypertensives only in acute stroke is given and commonly used IV (Intravenous) agents are also listed.   

Biography:

Abstract:

Autism spectrum disorder (ASD) is a neurodevelopmental syndrome that is marked by significant deficits in verbal and non-verbal social interactions, and by a peculiar pattern of restricted repetitive behaviors. Oxytocin is known for its involvement in mammalian social behavior and probably it might improve the symptoms of ASD. This research investigated the effects of intraperitoneal oxytocin on offspring of valproate-injected mothers during pregnancy. Animals were divided into five groups: control group (Con), control mice treated acutely with oxytocin (Con Oxy), autistic mice received normal saline (Au NS), autistic mice treated acutely with oxytocin (Oxy Ac), and autistic mice treated with oxytocin for two weeks (Oxy 2wk). In an elevated plus maze test, Con animals showed no anxiety-like behavior while Au NS mice showed anxiety-like behaviors. However, there was a positive improvement in anxiety-like behavior in Oxy 2wk group. Animals that were treated with oxytocin showed a clear tendency for  sociability and  social  novelty  in the three-chamber  test  used  to  test  social  behavior. There was an increase in the parameters measured by the behavioral spectrometry, the average velocity, activity and ambulation in Au NS group. On the other hand, all parameters were decreased in both Au Oxy groups with significant changes in Oxy 2wk group. Our data conclude that oxytocin causes significant reduction in anxiety and improvement of social interaction and autistic behavior when it was administered for two consecutive weeks. In the contrast, short term exposure to Oxytocin probably showed no significance difference in the results, which is suggested to be attributed to the stress effect of the intraperitoneal injection as well as the possibility for needing more time for oxytocin effect to be more prominent before testing

Biography:

Arthur G. O&#39;Malley worked as a consultant child and adolescent psychiatrist from 2004 to 2015 and am reaccredited as an EMDR consultant for Children, Adolescents and Adults from 2018 to 2023. I have also trained in sensorimotor psychotherapy. I have been a member of the UK and Ireland EMDR association since 2002 and was a member of the European Conference organizing committee for the London Conference and the Child and Adolescent Committee. I am currently a member of the child and adolescent committee of the UK and Ireland EMDR association with the portfolio for research. I have presented at their AGMs in Glasgow, Manchester, Dublin and at the European conferences in Paris and London. I have presently widely in the fields of trauma, neglect and the developing brain, attachment disorders, personality disorders, emotional dysregulation in ADHD and ASD diagnosis and management. I first presented on this model at the ISSTD 28^th Annual conference in Montreal November 2011. Recent articles on the clinical effectiveness of SF-EMDR psychotherapy have been published to complement the book. My first book, The Art of BART was published by Karnac books in London in 2015 and is available in print and as an eBook from Amazon and routledge.com. My new book, Sensorimotor-Focused EMDR: A New Paradigm for Psychotherapy and Peak Performance was published in December 2018. It will be officially launched on St Patrick’s Day 17 March 2019 at the Tim Parry Johnathan Ball Peace Centre, Peace Drive Warrington Cheshire UK

Abstract:

Lecture on Sensorimotor-Focused EMDR as a New Paradigm for psychotherapy and peak performance. This is an integrated approach to psychotherapy, which incorporates elements of trauma focused cognitive behaviour therapy (TF-CBT), Eye Movement Desensitization and Reprocessing (EMDR), mindfulness, somatic experiencing and sensorimotor psychotherapy (SP). This workshop gives participants an understanding of information processing in the body following significant life events. Gut feelings are initially registered at the level of the gut brain. Research on the gut microbiome and its relation to mental health will be presented. The next level of reprocessing takes place at the level of the heart brain, which is often linked to feelings of loss panic and anxiety. Activation of the body’s energy system continues with activation of the hypothalamic pituitary adrenal (HPA) axis. A key component of reprocessing is overcoming the symptoms of speechless terror, which are felt at the level of the throat and pharynx. The goal of activating and reprocessing these sensations, motor impulses, emotions, feelings and thoughts is to bring unconscious trauma triggers into conscious awareness. In trauma as Bessel van der Kolk wrote in 1992, “the body keeps the score”, with 90% of information stored somatically while we are consciously aware of only 10% of the information related to the traumatic event. This explains why premature use of CBT is ineffective. The reprocessing is continued with the patient being maintained in CALM WATERS (Conscious Aware, Level-Headed, Mindful, Window of Affective Tolerance Emotional Regulation and Stability). I will explain my two and three-dimensional models of dissociation associated with high arousal or RAPIDS (Racing Thoughts, Affective instability, Partitioned personality, Impulsivity, Distress and suicidality). This will also include a demonstration of dissociation and low arousal states or FROZEN in FEAR (Freeze Reaction, Oblivious, Zonked out, Emotionally Numb,  I will illustrate the use of the Sensorimotor EMDR psychotherapy with different types of traumatic dissociation with reference to individual cases of both acute and complex PTSD. I will also introduce delegates to quantum field theory and how quantum consciousness can be utilized in the consultation between therapist and client. The work of Professor Ernest Rossi in relation to the Basic Rest Activity Cycle during the therapist client interaction will be explained. This neatly ties into the work of Eckart Tolle in the Power of Now. I have been working intensively with a number of families with complex trauma and dissociation and will provide client feedback or patient reported outcome measures (PROM’s). I would like this patient-based evidence to be considered by the National Institute for Clinical and Health Excellence (NICE) as they produce guidelines for complex PTSD and dissociative disorders.

Biography:

Ben is a US-Certified Neuroscience Coach as well as a Neuro-Linguistic Programming (NLP) Master Practitioner. He is the Managing Director of Amplius Management Consultancy based in Manila, Philippines.  His firm provides services in the areas of Management Consultancy, Training, Organizational Development, and Market Research. He graduated with a degree in Engineering from the University of the Philippines.  Ben then proceeded to earn a Master of Business Administration (MBA) degree from the same university, and a Master of Science in Industrial Economics from the University of Asia and the Pacific. He has had an extensive Corporate Career in the different Functional Disciplines of General Management in a variety of Industries, such as Manufacturing, Sales & Marketing, Property Management and Development, Strategic Consultancy, and in a conglomerate involved in Shipping, Manning, and Business Process Outsourcing. Ben combines Science with Management Theory and actual Corporate Experience to design novel solutions to Organizational challenges. 

Abstract:

“Outsourcing” refers to the practice of outsourcing NonCore Business functions of an Organization to 3rd Party Business Process Outsourcing (BPO) Service Providers.  The Outsourcing Industry is one of the fastest growth industries in the World, with an average annual expansion rate of 20%.  And the Philippines is among the top countries of choice where BPO Service Providers locate. Its contribution to the Philippine GDP is approximately 19% in 2018 and it is the Philippines’ 2nd largest net foreign exchange earner and is the country’s most important generator of jobs.   Its workforce is dominated by Millennials whose office hours adjust to the time of the Clients (so Philippine BPOs catering to American Clients work from 8pm to 12noon).  This promotes a lifestyle rooted on insufficient sleep, lack of exercise, and a diet that thrives on coffee and fast foods.  Work is intensely stressful as strict compliance to Performance Metrics and Service Level Agreements are demanded. BPOs traditionally resort to providing non-monetary benefits such as regular special events, game rooms, and weekly massages in order to retain their people.  But “Worker Attrition” remains as its primary challenge, with an average 30% of its people leaving before their 6th month of employment. Neuroscience Concepts which contradict prevalent industry practices have successfully lowered Worker Attrition among my BPO Clients.  Using Lectures and Demonstrations, Coaching and Mentoring, Key Performance Metrics have been met through solutions which give rise to the optimal mix of the “DNA of Achievement”, namely; Dopamine, Noradrenaline, and Acetylcholine.  As a result, emotions have been regulated, focus has been sharpened, learning has been optimized, and a culture of trust has been established.  And analysis of field data reveals not that only has Worker Attrition gone down, but “Average Handling Time” (the time it takes to complete a Phone Conversation) has also decreased.