Scientific Program

Day 1 :

  • Neuroinflammation
Speaker
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. 

  • Neuroimmunology
Biography:

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.   

  • Neuroscience
Biography:

Abstract:

Patient satisfaction is one of the important indicators in the quality of health care. Iowa Satisfaction with Anesthesia Scale (ISAS) questionnaire is one of the robust questionnaires measuring patient satisfaction in anesthesia care. However, the Persian version of this questionnaire is not available. Therefore, this study examines the validity and reliability of the Persian version of the ISAS questionnaire. This questionnaire has 11 questions (3 questions about pain, 6 questions about patient experiences during the surgery, and 2 questions about satisfaction of patient). Patient pain is one of the most important factors that modulate the patient satisfaction in anesthetic care. Materials and Methods: In this clinical trial, 230 candidates for eye surgery with topical anesthesia entered the study. After obtaining informed consent, the Persian version of the ISAS questionnaire was completed during and one hour after the operation. Reliability, face, content, concurrent and criterion validity was evaluated. Results: The questionnaire was completed for 205 patients. The mean age was 68.26 ± 10.61, including 98 (47.8%) men and 107 (52.2%) women. The average ISAS scores of patients are 1.02± 0.65 and its range was -1.55-2.00. Cronbach's alpha coefficient was 0.71 and there was a positive and significant correlation between test-retest scores. Facial and content validity was approved. In addition, a significant correlation with the satisfaction of the surgeon and visual analog scale (VAS) scores was observed, which suggests concurrent and criterion validity. In this study the satisfaction of pain extensively was considered and compared with VAS. There was significant correlation between the ISAS questionnaire and VAS (r= -0.524, p=0.0001). Conclusion: The findings of this study confirm the validity and reliability of the Persian version of the ISAS in outpatient satisfaction of anesthesia cares. Furthermore, our data suggest that this questionnaire is completely useful for considering the patient satisfaction of anesthesia and pain.

 

 

Speaker
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.

 

  • Neuro-Degenerative Disorders
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.

 

  • Neurology
Speaker
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.

 


Speaker
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 1st degree relative affected, while the rest had a 2nd or 3rd 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). 1st 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.

 

Speaker
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.

 

  • Neuropsychiatry and Behavioral Science
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 28th 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.

 

Day 2 :

  • Stem cells & Neurological disorders

Session Introduction

Anila Benny

National Institute of Mental health and Neuroscience, India

Title: Neurological manifestations of vitamin B12 deficiency, CNS Manifestations
Biography:

Abstract:

Vitamin B12 (cobalamin) discovered at Merch , structural actualization by Hodgkin, Minot and Murphy’s hall mark study on treatment of cobalamin deficiency. Castle’s discovery on the gastric component ,intrinsic factor. And this is still the subject of intense research in its role in preventing the irreversible neurological lesions. A water soluble vitamin, involved in the metabolism of the body. A cofactor of DNA synthesis, metabolism of Amino acids and fatty acids, and vital in the normal functioning of CNS. According to current reports ,cobalamin deficiency are being most seen in developing countries than developed countries. The most frequent neurological manifestations of vitamin B12 Deficiency is sub acute combined degeneration of spinal cord.  Along With the symptoms of numbness, paresthesias  ,ataxia of gait, urinary incontience and urgency.   Other  CNS manifestations include optic neuropathy, peripheral neuropathy and Cerebral symptoms such as apathy ,depression, dementia, psychosis. An historical study by Reynolds et.al in 1992 founded that the low levels of cobalamin and be related with multiple sclerosis .  cobalamin deficiency can cause hyper homocysteinemia, which can be related to even stroke, MI, Premature atherosclerosis and venous thromboembolism. Laboratory diagnosis for this include serum cobalamin levels, schilling test and deoxyuridine suppression test etc. Vitamin B12 deficiency and causes both axonal and demeylidine changes ,is common occuring through the dietary   deficiency .blood smear test and bone marrow test are useful indication for the  possible vitamin B12  deficiency.              

 

  • Neuro-Degenerative Disorders
Biography:

Dr. Abdolhossein Parnow is assistant professor at exercise physiology. He has totally his expertise in work with physical activity and neuromuscular adaptations as well as he works on effects of physical activity and exercise training on people with Multiple Sclerosis disease and Migraine disorder. In this area, he investigate ways to be influence for these people to find economic ways that may improve the physiology function and quality of life. Since the physical activity has been shown has more advantages than other treatments, finding optimal exercise training types would be important outputs to access the goals.

 

Abstract:

Studies has been reported that regular aerobic exercise has cardiorespiratory benefits in the general population so that improves Vo2max and decreases O­2 consumption in rest and during submaximal activity such as walking. Physiological Cost Index (PCI), therefore, is a tool that measures energy cost during walking via the heart rate during walking activity, rest, and speed of walking (m/min). In addition, the dysfunction of Muscular and cardiorespiratory systems in people with Multiple Sclerosis (MS) leads to increase energy consumption cost during walking and decrease Vo2Max. MS is an autoimmune degenerative disease of the CNS and diagnosed in young adults between the ages of 20 and 40. Based on the body of evidence, recommendations have been made to include appropriate exercise prescription as an adjunct to MS treatment therapy. In addition, it has documented that PCI increases in people with MS since the HR increases during walking and at rest as well as walking speed decreases. Based on above reports, the higher value of PCI in MS results from cardiorespiratory and macular systems’ dysfunction. Our findings showed that regular aerobic exercise affects HR during walking and at rest and it improves walking speed and VO2Max in people with MS. These results, therefore, has been shows that physical activity could play main role in PCI improvement in people with MS. PCI probably helps neurologist, exercise trainers, and physiotherapist to plan optimal programs used as rehabilitation or prevention programs. By considering the benefits of physical activity, it would be presented the role of physical activity and PCI in people with MS in this workshops and be discussed how the exercise training should be design and execute.

 

  • Neuro Pharmacology

Session Introduction

sundas Hira

Riphah International University, Pakistan

Title: Effectiveness of beta carotene in streptozocin induced cognitive impairment in mice
Biography:

Sundas Hira is working as a lecturer at Riphah Institute of Pharmaceutical Sciences, Riphah International University. She is contributing dedicatedly her best part in research and publications. She has her expertise in assessing the use or effectiveness of natural substances in neurodegenerative diseases. Her research work based on “evaluating the effectiveness of beta carotene in streptozocin induced cognitive impairment in mice” probe the use of natural supplements in various disease resulting due to oxidative stress.

Abstract:

Several areas of brain are involved in regulation of memory. Of most important are amygdala and hippocampus. A number of antioxidants available are used for the treatment of many ailments. The present study was conducted to evaluate the effectiveness of exogenous antioxidant such as beta carotene (1.02 &2.05 mg/Kg) against ICV streptozocin induced memory impairment in mice. ICV streptozocin (3mg/Kg) was administered in two divided doses (on 1st and 3rd) for neurodegeneration. Male albino mice (n = 75) were used in the protocol which were further subdivided into five groups (Group I- control, Group II- diseased, Group III-standard, Group IV-V treated with beta carotene) to investigate the cognitive enhancement effect of selected antioxidant. Learning and memory behavior was assessed following the passive avoidance, elevated plus maze and open field paradigm. Biochemical markers of oxidative stress such as glutathione peroxidase, superoxide dismutase, catalase and acetylcholinestrase were analyzed in brain homogenates to evaluate the antioxidant potential and role of acetylcholine in memory enhancement. Results indicated that beta carotene at high dose (2.05mg/Kg) was more effective in the improvement of cognitive performance. It may be concluded from the study that beta carotene can be useful for memory enhancement and suggests its potential in the treatment of many neurodegenerative diseases such as Alzheimer’s disease 

  • Neurogenesis and Gliogenesis
Speaker
Biography:

Dr. Taylor joined the faculty as an Assistant Professor of Genetics in the Department of Biology in the College of Science, Engineering, and Technology at Jackson State University. While at JSU, Dr. Taylor is a Research Center for Minority Investigators (RCMI) faculty member, a graduate and undergraduate student advisor, mentor, and professor. She obtained her PhD in Microbiology from Indiana University, a Masters of     Science degree in Biology, from Jackson State University, and her Bachelors of Science degree in Biology from Tougaloo College. She was a Fellowship in Research and Science Teaching (FIRST) postdoctoral fellowship at Emory University in the Departments of Anesthesiology and Neurology. Her current research focus is determining the role of signal transducer activator of transcription 3 (STAT-3) on the regeneration of  nerve tissue and functional recovery after focal ischemic stroke. 

Abstract:

Wnt signaling is a conserved pathway involved in expansion of neural progenitors and lineage specification during development. However, the role of Wnt signaling in the post-stroke brain has not been wellelucidated. We hypothesized that Wnt-3a would play an important role for neurogenesis and brain repair. Adult male mice were subjected to a focal ischemic stroke targeting the sensorimotor cortex. Mice that received Wnt-3a (2 µg/kg/day, 1 hr after stroke and once a day for the next 2 days, intranasal delivery) had reduced infarct volume compared to stroke controls. Wnt-3a intranasal treatment of 7days upregulated the expression of brain-derived growth factor (BDNF), increased the proliferation and migration of neuroblasts from the subventricular zone (SVZ), resulting in increased numbers of newly formed neurons and endothelial cells in the penumbra. Both the molecular and cellular effects of Wnt-3a were blocked by the Wnt specific inhibitors XAV-939 and Dkk-1. In functional assays, Wnt-3a treatment enhanced the local cerebral blood flow (LCBF) in the penumbra, as well as improved sensorimotor functions in a battery of behavioral tests. Together, our data demonstrates that Wnt-3a signaling can act as a dual neuroprotective and regenerative factor for the treatment of ischemic stroke.