Scientific Program

Day 1

Neurology | Neuropsychiatry | Psychiatry | Neurological Disorders Neuroscience | Bipolar Disorders | Cognitive Neuroscience| Alzheimers Disease | Depression | Psychotherapy
Chair
Co-Chair
Speaker
  • Neuroprotective role of a small peptide derived from neuronal cell cycle like kinase (Cdk5) activator (p35)
    Speaker
    Harish C. Pant
    NINDS, NIH, USA
    USA
    Biography

    Dr. Pant received his M.A. and Ph.D. degrees in Physics from Agra University, Agra, India. His postdoctoral studies were conducted on the mechanisms of electron and ion transport in model membrane systems at the Department of Biophysics at Michigan State University. He joined the Laboratory of Neurobiology in the NIMH as a senior staff fellow in 1974 with Dr. Ichiji Tasaki where he studied the function of the axonal cytoskeleton in the squid giant axon. In 1979 he moved to the NIAAA extending his studies on the neuronal cytoskeleton and the effects of alcohol on its regulation. Dr. Pant moved to the NINDS, Laboratory of Neurochemistry in 1987 where he is presently chief of the section on Cytoskeleton Regulation. His laboratory is studying the mechanisms of topographic regulation of neuronal cytoskeleton proteins by post-translational modification, including the role of kinase cascades in normal brain and during neurodegeneration.

    Abstract

    Cdk5 is a member of cyclin-dependent kinases. It is unique among Cdk family of kinases; it is not activated by cyclins but is activated exclusively by the brain-specific p35/p25 proteins. It is a multifunctional protein kinase constitutively active in nervous tissues. It is implicated in ameliorating various neurodegenerative diseases phenotypes including AD. Cdk5, (Cdk5/p35), activity is tightly regulated and essential for nervous system development and neuronal functions. Emerging evidence suggests that its deregulation and hyper activation due to neuronal insults produced p25 and accumulation and aggregation of synaptic and cytoskeletal proteins in neuronal cells forming early stages of neurofibrillary tangles, plaques, Lewy bodies inclusions. These aggregated proteins and peptides are the hallmarks of AD, PD and ALS pathologies. On the basis of a large number of studies we have proposed Cdk5/p35 is a physiological and Cdk5/p25 is pathological target. To reduce the pathological phenotypes in situ / in vivo we discovered p5, a 24-amino acid truncated peptide from Cdk5 activator protein, p35, selectively inhibited the deregulated and hyperactive active Cdk5, (Cdk5/p25), induces pathology, but not Cdk5, (Cdk5/p35), kinase essential for nervous system development, function and survival. Recently it has been provided sufficient information that a modified truncated 24-amino acid peptide (TFP5), derived from the Cdk5 activator p35, penetrates the blood-brain barrier upon intraperitoneal injections (ip), inhibits significantly abnormal Cdk5 hyperactivity, and rescues significantly, AD pathology (up to 70–80%) in 5XFAD, p25Tg AD model. In addition, MPTP induced phenotypes in Parkinson’s disease model mice. The present talk will provide the molecular and cellular basis of the selectivity of these two forms of kinases, Cdk5/p35 and Cdk5/p25, physiological and pathological behavior of Cdk5/p35 and Cdk5/p25 kinases. We propose, TFP5 may be able to ameliorate several phenotypes in different neurodegenerative disease.

  • Assessment of effort and exaggeration during the neuropsychological examination
    Speaker
    Bob Gant
    Institute for Clinical Neurosciences
    USA
    Biography

    Bob Gant is a board-certified Clinical Neuropsychologist with extensive professional experience as a treating and Forensic Neuropsychologist, including the assessment of and treatment of brain injury and PTSD. He completed a clinical internship at the University of Kansas Medical Center and is the past President of section II of the APA Division of Clinical Psychology. He is a licensed Psychologist in two states (Colorado and Texas) in the United States. He is on the board of the American Board of Professional Neuropsychology (ABN) and Director of an approved Residency program in Clinical Neuropsychology (ACPN) in Boulder Colorado and Dallas, Texas.

    Abstract

    Clinicians who evaluate patients with neurological disorders including head injuries are often challenged to determine if the patient is providing poor effort or exaggerating symptoms. Rapid advances have assisted in this effort and there are multiple tools available now to assist the clinician in their assessment. These tools will be the focus of this presentation.

  • Beyond the art of BART: sensorimotor focused EMDR for psychotherapy and peak performance
    Speaker
    Dr. Shashita Inamdar
    University of Oklahoma Health Sciences Center
    USA
    Biography

    Shashita Inamdar is a licensed physician and board-certified child, adolescent and adult Psychiatrist. Inamdar is the Medical Director at Achieve TMS Centers and Achieve Concierge, renowned centers in San Diego, California for psychiatric, psychological and TMS treatment. She is also the Medical Director at the Center for Discovery, a leading residential and outpatient eating disorder treatment program. Inamdar serves as a member of the Advising Faculty at USD School of Nursing and Health Sciences. She also serves as a member of the Adjunct Clinical Faculty at Lake Erie College of Osteopathic Medicine, Department of Family Practice. Inamdar has over 20 years of extensive expertise in the diagnosis and management of emotional and psychiatric disorders. She is experienced in pharmacogenetic testing, ketamine treatment and neuromodulation treatments such as TMS and neurofeedback. She is currently engaged in developing a treatment program employing neuro-navigation and deep brain stimulation.

    Abstract

    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 (Freeze Reaction, Oblivious, Zonked out and 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.

  • Perspectives of nano-interventions in early diagnosis and treatment of Alzheimer’s disease
    Speaker
    Jerzy Leszek, M.D. Ph.D
    Wroclaw Medical University
    Poland
    Biography

    Dr Jerzy Leszek is Professor of Psychiatry, Vice-Head of the Department of Psychiatry , Head of Alzheimer’s Disease Lab at the Medical University in Wroclaw , and Scientific Director of Alzheimer’s Disease Center in Scinawa near Wroclaw, Poland. He graduated at Medical University of Wroclaw in 1979, was awarded a doctorate in Wroclaw in 1981 and in 1999- examination for the degree of associate professor of psychiatry and since 2005 he is working as full professor of psychiatry at Wroclaw Medical University. He is author and co-author more than 240 papers (especially from old age psychiatry), some chapters to the books published in reputed Polish and international journals and serving as an editorial board member of several journals .He is Editor –in-Chief of Journal of Yoga and Physical Activity. He is Scientific Editor and co-author of first Polish academic handbook on Alzheimer’s disease and nine another academic handbooks from old age psychiatry(Polish and internationals) , member a lot of scientific associations e .g founder and president of Lower Silesian Association of Alzheimer’s Families, first of its kind in Poland ,President of the Scientific Council of Alzheimer’s Disease Center in Scinawa, near Wroclaw , Former President and founder of Polish Psychogeriatric Association, Former Secretary(now member) of European Old Age Psychiatry and Former Member of Board of Directions of International Psychogeriatric Association

    Abstract

    The lack of effective treatment for Alzheimer’s disease (AD) stems mainly from the incomplete understanding of AD causes. Currently there are several hypothesis which try to explain the early molecular mechanisms of AD pathogenesis. The current pathophysiologic approach is based on a number of common mechanisms of neurodegeneration, including accumulation of abnormal proteins tau and ABeta), mitochondrial dysfunction, oxidative stress, impaired insulin signaling, calcium homeostasis dysregulation, imbalance of neurotransmitters, early synaptic disconnection and late apoptotic cell death. Considering that AD is a multi-factorial disease with several pathogenic mechanisms and pathways, a multifunctional nanotechnology approach may be needed to target its main molecular culprits. There are still no effective treatments to prevent, halt or reserve AD. To very early diagnosis of AD we need to have affordable, ultrasensitive and selective molecular detection methods. Nanomedicine as a biomedical and pharmaceutical application of nanotechnology for making Nano carriers for instance dendrimers has shown great potential not only for diagnosis but the treatment of many CNS diseases such AD. Ultra-low concentrations of protein biomarkers (eg.ADDL-amyloid-Beta-derived diffusible ligands) which have been implicated in the pathogenesis of AD, is possible to detect, owing to carrier dendrimers. Dendrimers are polymeric molecules chemically synthesized with well -defined shape size and nanoscopic physicochemical properties reminiscent of proteins. Recently an increasing number of studies have been focused on the potential dendrimers to prevent aggregation and fibrillation of proteins involved in neurodegenerative disorders such as AD. Some of dendrimers were demonstrated to cross blood-brain barrier, which legitimized research on these compounds as potential drugs for neurological disorders. Recent our studies have revealed that dendrimers possess the intrinsic ability to localize in cells associated with neuroinflammation (activated microglia and astrocytes) and thus can be used in neuroinflammation therapy. Above/mentioned findings may be significance in the context of potential application of dendrimers as drug carriers or active compounds per se. According to opinion the authors of this presentation, they are promising macromolecules for further investigations on their applicable in neurodegenerative disorders, for instance AD.

  • A new battle front against neuropathic pain
    Speaker
    Jorge Armando Bernal Zamora
    Technological Institute of Advanced Studies of Monterrey
    Mexico
    Biography

    Specialty Internal Medicine : 1992-1996 Monterrey NL , Hospital Universitario de Monterrey Universidad Autonoma de Nuevo Leon Specialty in Neurology 1996-1999 Hospital San Jose TEC de Monterrey TECHNOLOGICAL INSTITUTE OF ADVANCED STUDIES OF MONTERREY Master's Degree 1999-2000 Fellowship in Sleep Disorders Houston Tx. Training polysomnography and psycho disorders in sleep disorders 2010 Certification in treating non-motor symptoms of Parkinson enfe4rmedad Vancouver Canada 2011 Seminar in pharmacological treatment of motor symptoms and non-motor Parkinson Disease Toronto Canada 2012-2013 Diploma in mood disorders Málaga Eng. Diploma with specialization in mood disorders and psychopharmacology in depression and anxiety 2014 Diploma in Multiple Sclerosis treatment in Malaga Spain 2007, 2008, 2009, 2010, 2011, 2012, 2013 Congress of the Mexican Academy of Neurology. 2010, 2011.2013, 2014, 2016 Congress of the American Society of Movement Disorders 2015 Weill Cornell Neurology Seminar Salzburgo Autria 2016 Neurology Fellow Paracelsus Medical University Salsburg Austria 2016 Movement disorders seminar Paraselsus DanouHospital Vien Austriaç Work activity Clinical neurologist in private practice Director, Center for Nutritional Care SYNAPSIS Neurology and Internal medicine staff 1999-2014 INSTITUTO MEXICANO DEL SEGURO SOCIAL CERTIFICATIONS • Certified by the Mexican Association of Neurology • Certified by the Mexican Association of Internal Medicine • Member of the Mexican Association of Neurology • Member of the Movement Disorders Society ACHIEVEMENTS • 1991 Chief Medical Internal Hospital Universitario de Saltillo • 1997 First Place Winner in the Congress of Biomedical Research Technological Institute of Higher Studies in Monterrey • 1998 Chief Resident in Neurology

    Abstract

    Central Sensitization is a phenomenon of neuroplasticity that has been characterized by the presence of spontaneous or persistent pain, expansion of areas affected by pain, and qualitative sensory disorders that include allodynia and hyperalgesia. The Central Sensitization results from a series of functional and anatomical alterations in the CNS, some of them potentially irreversible, which may be responsible, at least in part, for the persistence of pain after the resolution of the triggering tissue injury. Clinical and experimental evidence shows that noxious stimuli can sensitize the central structures of the nerves involved in the perception of pain. Many outstanding clinical examples of these effects include amputees with pains in a phantom limb that are similar or identical to those felt in the limb before it was amputated, and patients after surgery who have benefited from preventive analgesia that blocks the limb. afferent alluvium induced by surgery and / or its central consequences, chronic low back pain, diabetic neuropathy and degenerative osteoarthritis. The experimental evidence of these changes is illustrated by the development of sensitization, by a phenomenon called WIND up that translates as winding or pushing the expansion of the receptive fields of the neurons of the central nervous system, as well as by the improvement of flexion reflexes and the persistence of pain or hyperalgesia after the contributions of the injured tissues. The perception of pain is not simply a moment-to-moment analysis of noxious afferent input, but involves a dynamic process that is influenced by the effects of past experiences. Sensory stimuli act on neuronal systems that have been modified by previous inputs, and behavior that is significantly influenced by previous memory events. A better understanding of the changes induced by central and peripheral lesions on harmful stimulation should lead to a new and improved clinical treatment for the relief and prevention of pathological pain and not only anti-inflammatory or narcotic analgesics in the treatment of chronic pain.Today we know the phenomenon of CENTRAL SENSITIZATION and its role in the perpetuity of CHRONIC NEUROPHATYC PAIN like phenomenon reversible and modifiable related to neuropathic pain, we have some medicines thant help susessful en the treatment of neuropathic pain.

  • Benefits of acute intermittent hypoxia for treating spinal cord injury
    Speaker
    Atiq Hassan PhD
    Avalon University School of Medicine
    Netherlands
    Biography

    Dr. Atiq Hassan obtained his PhD in Biomedical Sciences from University of Saskatchewan Canada in 2015 and Master's degree in Neurosciences, from the University of Calgary, Canada. He is a biomedical scientist, specialized in neuroscience with 15 years of experience in research and academic environment and currently teaching Neuroscience at Avalon University School of Medicine as an Associate Professor.

    Abstract

    Atiq Hassan obtained his PhD in Biomedical Sciences from University of Saskatchewan Canada in 2015 and Master's degree in Neurosciences, from the University of Calgary, Canada. He is a biomedical scientist, specialized in neuroscience with 15 years of experience in research and academic environment and currently teaching Neuroscience at Avalon University School of Medicine as an Associate Professor. During his PhD, He explored the potential benefits of Acute Intermittent Hypoxia (AIH) as a novel rehabilitation intervention for facilitating the behavioral recovery of forelimb function following cervical Spinal Cord Injury (SCI) in rats in safe and meaningful.

Day 2

Neuropathic Pain | Cognitive Neuroscience | Autism | Neurology | Neuro Immunology | Traumatic Brain Injury | Neurodiagnostic studies | Multiple Sclerosis| Mental Health | Neurosurgery | Neuroprotective Measures
Chair
Co-Chair
Speaker
  • Difference participation of korean female physical activity by life cycle
    Speaker
    Younshin Nam
    Duksung Women’s University
    South Korea
    Biography

    Younshin Nam is currently working at Duksung Women's University in Seoul, Korea. During 2015 February till now she became Director of Seoul Sports Council. During 2012, January to till now she is working as Advisory Committee of Korean Sports and Olympic Committee and Vice-President of Korean Society of Sport Policy also as Vice-President of Korean Sport Exercise Physiology.

    Abstract

    The frequency of physical activity and participating sport are different from the life cycle of women in Korea. Women in their teens, 20’s and 30’s have a significantly higher rate of 'never doing physical activity'. The lack of physical activity can lead to a health threat. Women in their teens and 20’s say that physical activity makes muscles and skeletons male-like and it makes hard to maintain their beauty (Nam Younshin, Ju Seung-hee, 2012). Women have different life cycle characteristics. Women experience different physical and mental experiences from men such as menstrual period, pregnancy period, childcare period, menopause period. At this level, women’s physical activity policies must be developed and promoted with considering women’s life cycle characteristics. The purpose of this study is to promote for regular physical activity as women’s life cycle.

  • Immunological grounds on exercise-induced food and physical allergies
    Speaker
    Yi sub Kwak
    Dong-Eui University
    South Korea
    Biography

    Yi-Sub Kwak Educational information includes: BS, 1992, MS, 1994, PhD, 2000, Yonsei University, Korea; Research Fellow, Yonsei University College of Medicine, 2000-2002. He was appointed as: Professor, 2003-, he also held a position as Head of Institute of Sport Science, 2007 he held a position of Chair, Graduate School and Department of Physical Education, 2009-, Don-Eui University; Managing Editor, Journal of Life Science, Busan, 2007-. Publications: Numerous articles in professional journals (in the fields of exercise science, exercise immunology, exercise nutrition, health and science and so on). His honours includes: Best professor in Dong-Eui University, 2005-2016; Excellence award, Beijing International Convention of Sports Science, 2006, he also received excellence Award, Yaubian International Convention of Sports Science, 2007. He is a visiting Fellow of Harris Manchester College, University of Oxford, 2008.

    Abstract

    Purpose: It is well known that physical activity is beneficial for people with positive results for physical status and mental wellbeing. However, physical exercise decreases the immune response and may induce an allergy anaphylaxis at some situation as follows. A common example is exercise-induced asthma, exercise-induced urticaria, exercise-induced anaphylaxis and FDEIAn. Generally, anaphylaxis is a severe, potentially fatal, hypersensitivity reaction of rapid onset. It is a dramatic clinical emergency. There are lots of etiologic factors of anaphylaxis, the principal immunologic triggers are foods, insect stings, and drugs. In recent, physical exercise is also related with the anaphylaxis. In this paper, we present the current views of physiological mechanisms underlying physical anaphylaxis within the context of exercise immunology. we also deal with a detailed two kinds of EIA (exercise-induced asthma, exercise-induced anaphylaxis) and exercise prescription and medical treatment for exercise-induced asthma, exercise-induced anaphylaxis and CU (chronic urticaria). Methods: At first, we analysed and presented the causes, symptoms, pathophysiology, testing, treatment and prescription of exercise-induced asthma, exercise-induced urticaria, exercise-induced anaphylaxis and FDEIAn through many experiments and references. Results: Exercise-induced asthma is a typical asthmatic attack which follows a strenuous exercise lasting five to 10 minutes in circumstances of dry and cold air situation. Avoid of exercise in that conditions and drug treatment (beta-2 adrenergic agonists) must preferentially be preventive. Physical urticarias are a unique subgroup of CU in which patients develop urticaria secondary to environmental stimuli. Common triggers include cold and heat temperature, water, sunlight and even physical exercise. it is responsible for approximately 20-30% of all cases of chronic urticaria. FDEIAn is induced by different types and various intensities of physical exercise, and this is distinct from food allergy. It is useful to test both in vivo and in vitro an extensive panel of foods. Avoidance of allergenic foods for at least four hours before exercise has prevented further episodes in all our patients with specific FDEIAn. Conclusion: It is concluded that anaphylaxis remains a continuous challenge for the diagnosis and treatment. The adequate management of anaphylaxis requires rapid diagnosis, implementation of primary and secondary prevention measures, and immediate administration of subcutaneous epinephrine. Furthermore, patient education is necessary to heighten awareness of the sign and symptoms of two kinds of EIA and FEDIAn.

  • Computational modelling for cognition expansion: making the invisible visible
    Speaker
    Alice Marascu
    Nokia Bell Labs
    Ireland
    Biography

    Alice Marascu is a senior research scientist at Nokia Bell Labs. Previously, she was a research scientist at IBM Research-Ireland, and held post-doctoral research roles at University of Trento-Italy, and INRIA Rennes Bretagne Atlantique-France. Her research spans natural language processing, large scale streaming data processing, large scale complex pattern recognition and mining, time series analysis. She has given multiple talks to industrial and academic audiences and published results in main conferences in the areas of big data, data mining, machine learning, query answering (VLDB, PVLDB, SIGMOD, Big Data Conference, etc.).

    Abstract

    Artificial intelligence is reshaping our world and we assist at unprerceeding acceleration rates in numerous human activities. The core goal is the expansion of the human cognition, from its internal expansion (cognitive psychology) to its external expansion (social cognition). Understanding the complexity of the human brain and replicating its functionalities has been the goal of many scientists, and today, more than any time in the scientific history, the researchers are working on a more ambitious step of amplification and augmentation of cognition capabilities. We looked at the deep mental process triggering the human behaviour and building our personal behavioural print. We translated and adapted core psychology theories of human cognition into computational models. A digitisation of the mental processes opens the door to building a better self for self-cognitive capacities expansion, and equally important, a better relational self for augmented social cognition. We were interested in our personalised cognitive behavioural print and how it impacts our cognitive expansion. We will present our computational modelling and how we are testing it in real world applications.

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