International Conference on Brain Disorders and Therapeutics August 24-26, 2015 London, UK

Biography:

Psychologist w firmie University of Social Sciences and Humanities

Abstract:

The research aims to investigate the functioning of the brain at an early age, while taking into consideration the role of working memory and stimulating the function. We explored the cognitive profiles of children with working memory impairments. In an initial screening of 180 six-year-olds and identified children with low working memory scores. The research includes 2 groups of children: active (with cognitive training) and passive (without cognitive training). Cognitive skills (Raven's Coloured Progressive Matrices (CPM) - psychological test, Antisaccades (AS) task, Memory Guided Saccades (MGS) – eye-tracking research, Test of Working Memory Capabilities (TOWMC), Test of Knowledge and Competences (TOKAC) were assessed before, after cognitive training and third time, tree months after cognitive training). The training took 8 weeks, 5 times a week, 15 – 20 minutes each day. We studied the hypothesis: 1.The improvement of the trained function of operational memory measured by the eye-tracker will be noted in all training groups, but a higher dynamic of progress will be observed among children with low working memory; 2. The transfer of the effects of cognitive training will be observed in eye-tracker, TOWMC and TOKAC data, but among children with low working memory it will be more differentiated, than among healthy children; 3. The improvement of learning skills measured by TOKAC will be noted in all training groups, but a higher dynamic of progress will be observed among children with low working memory; 4. Durability of the training results on the operational memory’s functioning will be observed in all groups. The results of the research should serve as a basis for further studies, both cognitive and clinical. In cognitive studies, they should serve as a reference point to further studies into the role of working memory and cognitive training in early development stage. In clinical studies, the effects of the experiment can serve an important role in combining computer cognitive training with another treatment e.g. medication.

Biography:

Hans von Holst received his Medical Doctor´s degree in 1976 at Karolinska Institutet and completed his specialist training in Neurosurgery 1982 at Karolinska University Hospital. In 1985 he earned his PhD when he also became Associate Professor in Neurosurgery, Clinical Neuroscience at Karolinska Institutet. Since 1988 he holds a position as Senior Physician in Neurosurgery at Karolinska University Hospital. During 1991-1996 he was appointed as Chairman of the Dept of Neurosurgery and Division Manager of the Neuroclinics at Karolinska University Hospital, respectively. From 1992 to 2006 he was appointed as chairman of the World Health Organization collaborating center for neurotrauma at Karolinska Institutet. Since 2003 he is Professor in Neuroengineering and Head of the Division of Neuroengineering at the Royal Institute of Technology in Stockholm. He has over 120 original research publications, book chapters and books

Abstract:

Cytotoxic brain tissue edema is a complicated secondary consequence of ischemic injury following traumatic brain injury and stroke. The pathophysiological mechanisms are known to some extent but far from completely. A hypothesis has been proposed where protein unfolding and perturbation of nucleotide structures participate in the development of cytotoxic edema. The hypothesis is based on an advanced computational simulation model of the human head where a simulation of a traumatic brain injury was performed. The consequences of kinetic energy transfer following an external dynamic impact were analyzed including the intracranial pressure (ICP), strain level, and their potential influences on the noncovalent and covalent bonds in folded protein structures. It was shown that although most of the transferred kinetic energy is absorbed in the skin and three bone layers. It was further discovered that a substantial amount of kinetic energy reached the the brain tissue in gray and white matter. Thus, the kinetic energy from a dynamic impact has the theoretical potential to interfere not only with noncovalent but also covalent bonds when high enough. The induced mechanical strain and pressure may further interfere with the proteins. Simultaneously, the noncovalent energy rich bonds in nucleotide adenosine-triphosphates may be perturbed as well. The subsequent attraction of increased water molecules into the unfolded protein structures and disruption of adenosine- triphosphate bonds could to some extent explain the etiology to cytotoxic edema. Based on the new hypothesis and knowledge it is realistic to change the neurosurgical treatment of today by using neuroengineering simulations already before a neurosurgical procedure is taking place. Further development of the innovative hypothesis makes it possible to open up for new drug and infusion treatment aiming at redicing the severe consequences of cytotoxic brain tissue edema.

Biography:

Miriam Furst received the B.Sc. and M.Sc. degrees in applied mathematics and the Ph.D. degree in biomedical engineering from Tel Aviv University, Ramat Aviv, Israel, in 1973, 1975, and 1981 respectively. From 1982 to 1984, she was a Post-DoctoralFellow in the Research Laboratory of Electronics, Massachusetts Institute of Technology (MIT), Cambridge. Since 1984, she has been a faculty member with the Department of Electrical Engineering Systems, Tel Aviv University. Her main research interest is the auditory system as part of a wider interest in human communication channels. She has published more than 50 papers.

Abstract:

Multiple sclerosis (MS) is a disease that is both a focal inflammatory and a chronic neurodegenerative disease. The focal inflammatory component is characterized by destruction of central nervous system myelin including the spinal cord; as such it can impair any central neural system including the auditory system. While on the one hand auditory complaints in MS patients are rare compared to other senses, such as vision and proprioception, on the other hand auditory tests of precise neural timing are never “silent.” Whenever focal MS lesions are detected involving the pontine auditory pathway, auditory tests requiring precise neural timing are always abnormal. Azimuth sound localization is accomplished by comparing the timing and loudness of the sound at the two ears. Hence tests of azimuth sound localization must obligatorily involve the central nervous system and particularly the brainstem. Whenever a focal lesion was localized to the pontine auditory pathway, timing tests were always abnormal. A timing test that included only high frequency sounds was very often abnormal even when there was no detectable focal MS lesion involving the pontine auditory pathway. This test may be a marker for the chronic neurodegenerative aspect of MS, and, as such could be used to complement the MRI scan in monitoring the neurodegenerative aspect of MS. Studies of MS brainstem lesion location and auditory function have led to advances in understanding how the human brain processes sound. The brain processes binaural sounds independently for time and level in a two stage process. The first stage is at the level of the superior olivary complex (SOC) and the second at a level rostral to the SOC.

Biography:

Alex Bekker is an internationally recognized expert in neuroanesthesia and is frequently invited to speak at Grand Rounds and Scientific Panels. He has been active in research for many years. He is the author of 62 peer reviewed publications, 6 US patents, 32 educational reviews and more than 100 abstracts. His work has focused on perioperative brain protection, neuroinflammation, and clinical pharmacology. He was a PI of numerous clinical trials, including studies sponsored by the National Institute of Aging. He serves on the editorial board of the Journal of Neurosurgical Anesthesiology and is an ad hoc reviewer for 15 peer-reviewed journals, including NEJM, Anesthesiology, Neurosurgery, and Anesthesia and Analgesia. He is spearheading a campaign to improve the efficiency of Perioperative Services as well as Patient Safety at the University Hospital

Abstract:

Perioperative stroke is defined as an episode of focal or global loss of cerebral function with symptoms lasting more than 24 hours. Perioperative strokes result in increased duration of hospital stay, rates of disability, discharge to long-term care facilities and death after surgery. General surgical procedures are associated with a 0.08-0.7% risk of stroke. The incidence is higher for coronary artery bypass grafting surgery (1.4-3.8%) and valve replacement surgery (up to 9.7%). Potential stroke etiology includes hypoperfusion (global and focal), thromboembolism and hemorrhage. The preoperative patient related risk factors for perioperative stroke are advanced age, previous cerebrovascular diseases, peripheral vascular disease, chronic obstructive pulmonary disease (COPD), atrial fibrillation, hypertension, cardiac valvular disease, diabetes mellitus, HTN, atherosclerosis and renal disease. General anesthesia, dehydration, bed rest, stasis in the postoperative period and perioperative withholding of antiplatelet or anticoagulation agents can aggravate surgery-induced hypercoagulability and increase the risk of perioperative thrombogenic events. Elective surgery should be delayed for at least 1 month after a documented ischemic stroke. Another consideration in the preoperative period is patients who require chronic anticoagulation. Bridging oral anticoagulant therapy (warfarin) with heparin or low molecular weight heparin should be considered for the majority of patients who require temporary interruption of warfarin therapy. Several studies suggested that intraoperative hypotension induced by anesthesia does not considerably increase risk for perioperative stroke in patients with carotid disease. Most authors recommend that intraoperative blood pressure should be maintained within 20% of preoperative level.Postoperative risk factors for a stroke include heart failure, myocardial infarction, arrhythmias (atrial fibrillation), dehydration (blood loss) and hyperglycemia. Anticoagulation in the immediate postoperative period especially in patients with AF may be useful.Implementation of the therapeutic measures that reduce the incidence of this complication is an appealing concept because failure of neuroprotective agents in acute stroke may be due to delay in presentation after stroke has occurred. Preoperative administration of statins, ASA, a continuation of anticoagulation therapy (when indicated) as well as appropriate timing of surgery do appear to reduce the incidence of stroke after CABG and vascular surgery and may show similar results in the general surgery population as well. Anesthesiologists can implement several therapeutic and procedural measures to minimize morbidity associated with a perioperative stroke.

Biography:

Michihiko Koeda is a senior assistant professor of the psychiatry department at Nippon Medical School, Tokyo, Japan. He completed his PhD at the Medical Research Institute of Tokyo Medical and Dental University. He was a visiting researcher at the University of Glasgow. He is continuing to investigate auditory brain function by the use of functional MRI to clarify the pathophysiology of psychiatric symptoms, and pharmacological and/or genetic effects

Abstract:

Greeting conversations are essential tools for communicating socially with family, friends, and community. Attractiveness is one of the favorable behaviors associated with social communication. A recent study showed that the roles of inferior frontal gyrus (IFG) and superior temporal gyrus (STG) are essential for perceiving auditory attractiveness. However, to our knowledge, no study has ever investigated the cerebral response to auditory attractiveness in schizophrenia. We aimed to clarify the cerebral function underlying the perception of auditory attractiveness in schizophrenia patients. Cerebral activation was examined in 18 schizophrenia patients and 18 controls when performing Favorability Judgment Task (FJT) and Gender Differentiation Task (GDT) for pairs of greetings using event-related functional MRI. Full-factorial analysis revealed that the main effect of task was associated with activation of left IFG and STG. The main effect of Group revealed less activation of left STG in schizophrenia compared with controls, whereas significantly greater activation in schizophrenia than in controls was revealed at left middle frontal gyrus (MFG), right temporo-parietal junction (TPJ), right occipital lobe, and right amygdala (p<0.05, FDR-corrected). A significant positive correlation was observed at right TPJ and right MFG between cerebral activation under FJT minus GDT contrast and the score of hallucinatory behavior on the Positive and Negative Symptom Scale. Findings of hypoactivation in left STG could indicate brain dysfunction in accessing vocal attractiveness in schizophrenia, whereas hyperactivation in right TPJ and MFG may reflect the process of mentalizing other person’s behavior by auditory hallucination by abnormality of cognitive bias.

Biography:

Amir Mufaddel has graduated from Khartoum University and had his MD in psychiatry from Sudan Medical Specialization Board in 2008. Currently working in AlAin hospital, Community Mental Health Services. He is an adjunct lecturer in United Arab Emirates University. He has published several papers in reputed journals mostly reflecting the psychiatric aspects of physical conditions such as neurology, infectious diseases and dermatology.

Abstract:

The relation between psychiatry and epilepsy remains one of the topics that has been continuously attracting attention in medical literature since the time of Hippocrates. Forced normalization was later conceptualized when biological treatment for psychiatric disorders was developed. Recently, several reports were published regarding possible adverse psychiatric effects of antiepileptic medications. The picture is further complicated by the fact that psychotropic medications, which may be used for treatment of psychiatric disorders in epilepsy, can have negative effects on seizure control. Psychiatric symptoms, in relation to seizure, can be categorized into the following types: pre-ictal, ictal, post-ictal, inter-ictal and ictal symptoms. Depression and anxiety are commonly associated with epilepsy and can occur in all of the above categories . Depression can be severe and suicidal behavior has been reported as one of the common psychiatric associations with epilepsy, and has also been linked to use of some antiepileptic drugs. Psychosis can occur as an acute or chronic form. Transient pleomorphic post-ictal psychosis particularly observed in those with hippocampal sclerosis. There is an increased risk of developing schizophrenia and schizophrenia-like psychosis in patients with epilepsy. Psychiatric symptoms can also emerge during use of some of the antiepileptic drugs. Adverse psychiatric events include depression, psychosis, suicidal risk, and cognitive impairment. On the other hand, some of the psychotropic medications are known to be epileptogenic. Therefore, selection of psychotropic medications should be based on their possible effects on seizures; and those known to be epileptogenic should be avoided.

Biography:

Wayne Grant Carter received his Honors degree and PhD in Biochemistry from the University of Southampton, studying protein post-translational modification and molecular signalling cascades. He is currently a Group Leader in the School of Medicine, University of Nottingham, with research focused upon protein post-translational modification and molecular mechanisms of hepato- and neuro-toxicity.

Abstract:

The mechanism by which neurotoxicants, such as alcohol, damage neurons is not fully understood. To investigate the neuropathology arising from cumulative excessive alcohol consumption we examined prefrontal cortex brain tissue from human alcoholics and age, gender, and post-mortem delay matched control subjects. H&E staining and light microscopy of prefrontal cortex tissue revealed a reduction in the levels of cytoskeleton surrounding the nuclei of cortical and subcortical neurons, and a disruption of subcortical neuron patterning in alcoholic subjects. One dimensional polyacrylamide gel electrophoresis proteomics of cytosolic proteins identified dramatic reductions in the protein levels of spectrin β II, and α- and β-tubulins in alcoholics, and these were validated and quantitated by Western blotting. In alcoholics, significant loss of cytosolic α- and β-tubulins was also seen in the other brain regions examined: Caudate nucleus, hippocampus, and cerebellum. Collectively, our results suggest that the cytoskeletal architecture is notably susceptible to alcohol-related brain damage. Whether this represents a common pathological hallmark of neurotoxicants will be discussed.

Biography:

Sha Mi obtained her Ph.D. in Molecular and Cellular Biology from Rutgers University and her postdoctoral training in the laboratory of Dr. Richard Roberts (Nobel Laureate) at the Cold Spring Harbor Laboratory. Her major interests include the identification of novel CNS specific proteins involved in the regulation of neuronal cell survival, axonal regeneration, neuronal damage repair and remyelination. Her current focus is to identify therapeutics for the treatment of demyelination diseases such as MS. Her group is the first to identify proteins, LINGO-1 and DR6, that block remyelination repair in laboratory tissue culture and in animal disease models, and whose inhibition will allow for re-myelination and repair of damaged axons.

Abstract:

• LINGO-1 is a Leucine rich repeat, Ig domain containing, Nogo receptor interactive protein that is selectively expressed in CNS oligodendrocytes and neurons. Its expression is developmentally regulated, as well as up-regulated in CNS diseases and spinal cord injury. LINGO-1 negatively regulates oligodendrocyte differentiation and myelination, neuronal survival and axonal regeneration by activating RhoA and inhibiting ATK phosphorylation. Across diverse animal CNS disease models, targeted LINGO-1 inhibition promotes neuron and oligodendrocyte survival, axon regeneration, oligodendrocyte differentiation, remyelination and functional recovery. The targeted inhibition of LINGO-1 therefore represents a novel approach for the treatment of neurological diseases. BIIB033 is the first anti-LINGO-1 anti-body to enter clinical development for CNS repair. The Phase I study found anti-LINGO-1 to be safe and well tolerated up to the maximum planned dose of 100mg/kg. BIIB033 is currently being evaluated in Phase II clinical study for the treatment of RRMS and SPMS

Biography:

Bekker is an internationally recognized expert in neuroanesthesia and is frequently invited to speak at Grand Rounds and Scientific Panels. Dr. Bekker has been active in research for many years. He is the author of 62 peer reviewed publications, 6 US patents, 32 educational reviews and more than 100 abstracts. His work has focused on perioperative brain protection, neuroinflammation, and clinical pharmacology. Dr Bekker was a PI of numerous clinical trials, including studies sponsored by the National Institute of Aging. He serves on the editorial board of the Journal of Neurosurgical Anesthesiology and is an ad hoc reviewer for 15 peer-reviewed journals, including NEJM, Anesthesiology, Neurosurgery, and Anesthesia and Analgesia. Currently, Dr Bekker is spearheading a campaign to improve the efficiency of Perioperative Services as well as Patient Safety at the University Hospital

Abstract:

The brain is vulnerable during the perioperative period. Neurobehavioral disturbances are common complications of surgery, manifesting in three distinct forma: emergence delirium, postoperative delirium, and POCD. The relationship between these conditions has yet to be fully elucidated. Although not limited to geriatric patients, the incidence and impact of both are more profound in geriatric population. Delirium has been shown to be associated with longer and more costly hospital course and higher likelihood of death within 6 months or postoperative institutionalization. POCD is a condition characterized by deterioration of cognitive performance after surgery presenting as impaired memory and/or concentration. Perioperative physiological derangements (e.g. hypotension), anesthetics, duration of surgery, respiratory complications have been suggested as possible causes, but only age and limited education has proven to be consistent risk factors in most studies. Current research suggests that patients with preoperative cognitive impairment are at higher risk for POCD because of their already compromised status and their potential vulnerability to worsen into dementia due to a less cognitive reserve. In this presentation, we review the definitions, etiology, prevention and treatment of both disorders in patients undergoing major non-cardiac surgery.

Biography:

Naseer nadim completed his MD in 1982 from Sackler School of Medicine, Tel-Aviv. Previously he was working as Paediatric Residency & specialty at Porya Hospital, Tiberias, Rambam and Naharya HospitalS successively. Currently he is conducting a research on Periodic Fever at Clalit Health ORG. He is an honourable member of the European Society of Pediatric Cardiology and the Israeli Heart society

Abstract:

There is a considerable impression that the clinical descriptions of diseases of the white matter still suffers from vagueness and lacks organization, thus leaving the diagnosis of these disorders yet in a state of uncertainty. It is possible that the reason for opacity of these diseases is the widespread distribution of white matter through the body; from cerebrum till the nerve fibers endings in periphery; making the description of their injury symptoms and signs, despite being true, to be burdened by a list of scattered different details in a non-systematic manner, and lacking a pathognomonic sign, or a combination of signs, that could direct the clinician to diagnose a specific myelination disorder. Though, the distinction between central and peripheral nervous system disorders has been well established, by the finding of hyperreflexia in the former and areflexia in the later. The recently published; “MAIS-NADIM NASSER triad”, or (MNN triad), is a simple, but solid marker, based upon injury to three brain organs; first, the white matter in the brain’s sub-cortical sites, second the brainstem, and third are the optic nerves and tracts. It is assumed that a mutational myelination disorder of the central nervous system usually hits all the above mentioned three sites at the same time, or sometimes sequentially, sometimes after long periods between one and the other; thus causing the appearance of three major signs in the same order of the injuries occurrence. Based on the above information one can conclude that clinicians should follow up patients who suffer from one single sign; truncal hypotonia, for example, or sensorineural deafness, or nystagmus, and wait for the appearance of the two other signs of the MNN triad, so LD diagnosis at hand.

Biography:

Benjamin Van Voorhees, MD, MPH, is currently an Assistant Professor and the Interim Head of the Department of Pediatrics at the University of Illinois at Chicago Children’s Hospital. He received his BA in History from Dartmouth College, his Doctor of Medicine from Vanderbilt University, and his Master of Public Health from Johns Hopkins. He completed a Combined Internal Medicine-Pediatrics Residency at Vanderbilt University Hospital and a General Internal Medicine Fellowship at Johns Hopkins. He has received several grants ongoing research support (RDJF, NIMH, NARSAD, CMS, and CDC since 2002)—two will take special notice: (1) From NIH he has an R01 for Primary Care Internet-Based Depression Prevention for Adolescents (CATCH-IT) from 1/15/11-5/31/16. This a randomized clinical trial to determine if a primary care internet-based depression prevention intervention (CATCH-IT 2R) can build resiliency and protect adolescents (ages 13-17) against depression and strengthen their ability to attain their life goals. In 2014 his CMS grant, University of Illinois CHECK (Coordination of HEalthcare for Complex Kids) grant from 09/01/2014 - 08/31/2017 received total funding of $19,581,403. CHECK seeks to provide comprehensive, highly-innovative community-based care to 6000 children and young adults enrolled in Medicaid in Cook County, Illinois. CHECK is designed to improve care for populations with specialized needs, with a focus on the specific priority area of high-cost pediatric and young adult populations.

Abstract:

Efforts to prevent depression have become a key health system priority. Currently, there is a high prevalence of depression among adolescents, and treatment has become costly due to the recurrence patterns of the illness, impairment among patients, and the complex factors needed for a treatment to be effective. Primary care may be the optimal location to identify those at risk by offering an internet-based preventive intervention to reduce costs and improve outcomes. Few practical interventions have been developed. The models for Internet intervention development that have been put forward focus primarily on the Internet component rather than how the program fits within a broader context. This paper describes the conceptualization for developing technology based preventive models for primary care by integrating the components within a behavioral vaccine framework. CATCH-IT (Competent Adulthood Transition with Cognitive-behavioral, Humanistic and Interpersonal Training) has been developed and successfully implemented within various health systems over a period of 14 years among adolescents and young adults ages 13-24. We describe more than a decade of technology development, clinical trials and investigations into mechanisms of action for this “technology based behavioral vaccines”.

Biography:

Priscilla Chukwueke obtained her medical degree from American International School of Medicine, Guyana, South America, and has a Master’s degree in public health. She is currently pursuing her psychiatry residency at Harlem Hospital /Columbia University in New York, USA. This case report was done in conjunction with a neurologist- Dr. Anne Kleiman and a radiologist- Dr Leszek Pisinski all from Harlem Hospital / Columbia University and it has been published in clinical Neuropsychiatry journal in June 2015. She has presented posters nationally and internationally e.g. at The World psychiatric Congress in Madrid Spain in 2014.

Abstract:

Marchiafava-Bignami Disease (MBD) is a rare central nervous system (CNS) disease characterized by demyelination of the corpus callosum. It is mostly found in men with alcohol use disorder and malnutrition with cases reported worldwide across all races. The onset of the disease may be sudden presenting with stupor, coma or seizures while some may present with gait abnormality (spasticity), psychiatric problems, hemiparesis, aphasia, apraxia and incontinence with a resultant high morbidity and mortality rates. Case description: patient is a 30 year old left handed African-American, who presented with c/o altered mental status, urinary incontinence, slurred speech and left-sided weakness. The diagnosis of MBD was confirmed with DTI Tractography which showed significantly Diminished commissural fibers extending to the right central semiovale lesion, near absent or significantly diminished commissural fiber extending through the corpus callosum indicating demyelination. Discussion: MBD is often an incidental diagnosis with high morbidity and mortality. This is different from previous casas because of earlier onset as opposed to onset around age 45, rapid recovery and minimal disability as he could walk independently before discharge from hospital. This case also shows added benefit of the DTI tractography in the diagnosis of MBD.

Biography:

Abstract:

Biography:

After his BSc Honours and an MSc in theoretical mathematics, Professor Toro obtained a PhD in computational mathematics applied to fluid dynamics. Since then, much of his research has been centred on the numerical analysis of partial differential equations and aerospace, industrial, environmental and medical applications. He is author of almost 300 works and has received several awards, including two honorary doctorates and the honorary title OBE from her majesty The Queen Elizabeth II. Prof. Toro’s current research is focused on the bio-physics of neurological diseases and their potential link to venous haemodynamics and transport across the blood vessel wall

Abstract:

Recent medical research has identified a strong association between some pathologies of the central nervous system and anomalous cerebral venous haemodynamics. Such pathologies include Retinal Abnormalities, Transient Global Amnesia, Transient Monocular Blindness, Meniere’s Disease and Idiopathic Parkinson\'s Disease. Here we focus our attention on the biophysics of the circulation to address some of the questions raised regarding some of these brain pathologies, one of them being the hypothesis of brain venous hypertension. Such hypothesis is difficult, if not impossible, to prove through direct invasive measuring methods. Here we adopt a theoretical approach to study the problem, through a mathematical model for the full human circulation [1], [2], [3]. The model includes sub-­‐models for the arterial system, the microvasculature, the venous system, the heart and the pulmonary circulation. The model adopts a geometric multi-­‐scale approach comprising 1D models for major vessels and 0D models for the remaining components. Particular attention is paid to the brain venous system, allowing for the use of MRI-­‐acquired patient specific geometries and adopting a refined representation of the cerebral venous network, including models for the Starling-­‐like behaviour of cerebral veins and admitting the interaction of the blood with the cerebro spinal fluid. The model has been validated by using available data in the literature and specially obtained in vivo MRI cerebral flow quantification data. In this paper we apply our mathematical model to demonstrate that extra-­‐cranial venous strictures, such as malfunctioning valves and stenosis, cause intracranial venous hypertension. We show results of relevance to Meniere’s Disease, Idiopathic Parkinson\'s Disease and Multiple Sclerosis. We speculate on the potential clinical implications.

Biography:

Jan Hemza is currently working at Brno Epilepsy Centre at the Department of Neurosurgery at the Masaryk University

Abstract:

Our study about new physiological quality of vessels (angiosynizesis, self-excitation all vessel vibration), the movement of brain and flow of cerebrosinal fluid (effect of movement and exachanges during time of verbral column, especially 3D exchanges vertebral column canal) together go to realisation that the pulsing flow in live organism is essential. All study have similar design: experimental study, mathematical models, experimental models. Pulsing flow isn´t, e.g. the problem nonpulsing flow at arteficial pump in blood circulation, during time delay ischemic tissue deposit will be developed. The vibration of vessel wall during physiological state, facility begining of angiosynizesis by propagation pulsing pressure wave, structural stability of bridging veins can be restore by adequate rise in pressure in given moment. Pulsing system have a more side effects, maybe to electromagnetic continuum into live organism on remodeling live organism during life and on thermodynamic dissipation. The venous brain system has active and regulatory function in hemodynamic flow of brain

Biography:

Nan-Shan Chan completed his Ph.D on Immunology in 1984 from Medical University of South Carolina and currently he is an acting Director for the Institute of Molecular Medicine in the College of Medicine at National Cheng Kung University where his research is focused on elucidating the functional interactions between cancer cells and the innate immune system. How cancer cells evade immune attack and prevent death-inducing factors-initiated apoptosis has been our focus of research. To understand how cancer cells develop resistance to tumor necrosis factor (TNF), we have utilized functional cloning and microarray approaches to isolate genes, which may regulate cancer cell sensitivity to toxic cytokines. We have recently discovered a tumor suppressor WOX1 (also named WWOX or FOR), which enhances TNF function and is apparently involved in embryonic cell differentiation and cancer pathogenesis.

Abstract:

Substantial evidence reveals that tumor suppressor WW domain-containing oxidoreductase (known as WWOX, FOR or WOX1) blocks the progression of Alzheimer’s disease (AD). We have first demonstrated that WWOX binds tau and tau-hyperphosphorylating enzymes GSK3, ERK and JNK1, and thereby inhibits tau hyperphosphorylation (JBC 279:30498, 2004; Cell Death Differ 19:1049, 2012). In addition, WWOX promotes neuronal differentiation. Unfortunately, WWOX is frequently downregulated in the AD hippocampi (JBC 279:30498, 2004). And, this downregulation results in spontaneous aggregation of TIAF1 and TRAPPC6A, which leads to caspase activation, tau aggregation, APP degradation, formation of amyloid  and plaques in humans and in Wwox gene knockout mice (Cell Death Dis 1:e110, 2010; Oncotarget 6:3578, 2015). When WWOX protein is lost due to alteration of WWOX/Wwox gene such as missense or nonsense mutation and deletion, this leads to ataxia, epilepsy, dementia, neurodegeneration, diseases associated with HDL lipid metabolism, and early death in humans, mice and rats (Oncotarget 5:11792, 2014; Exp Biol Med 240:400, 2015). Our studies revealed that significant upregulation of proteins, which are involved in neurodegeneration, is found in the cortex and hippocampus of Wwox gene knockout mice. These proteins include GSK3, ERK, pERK, JNK1, pJNK1, TIAF1, pS35-TIAF1, TRAPPC6A, pS37-TRAPPC6A, -synuclein, C9orf72, TDP-43 and others. Notably, a zinc finger-like peptide Zfra is able to ameliorate the symptoms of AD in the triple transgenic mice, including neuronal death and memory and learning capabilities, suggesting its potential use in therapy for AD. (supported by DoD, USA and MOST and NHRI, Taiwan)

Biography:

Michele Mishto is a postdoc since 2005. He is currently working in the group of Peter Kloetzel (Institut für Biochemie, Charité Berlin). His main interests are proteasome isoforms functions with outcomes on: (i) neuroinflammation and its involvement in neurological diseases such as AD, MS and epilepsy; (ii) tumors; (iii) antigen presentation and immune response. He has 31 publications in peer-reviewed international journals (15 as first or last author) and H-index = 16.

Abstract:

The proteasome is the core of the ubiquitin proteasome system and is involved in several cellular metabolisms. The incorporation of three inducible immuno-subunits into the proteasome results in the generation of the so-called immunoproteasome, which is endowed of pathophysiological functions related to immunity and inflammation. We have shown that immunoproteasome is almost absent in healthy human brain, while it is induced in the patients affected by Alzheimer disease (AD), multiple sclerosis (MS) and temporal lobe epilepsy (TLE). The expression of immunoproteasome in the brain can affect the microglia activity in AD model, the neuronal activity in TLE animal models and the presentation of myelin antigens involved in MS. Immunoproteasome can affect the neuroinflammation by acting not only as intracellular but also as extracellular protease. Indeed, we show that extracellular proteasome seems to be involved in the regulation of the pleiotropic cytokine osteopontin, thereby playing a role in the development of relapse in RRMS patients. Recent studies on animal models identified immunoproteasome subunits as potential targets for treatment of MS and pharmaco-resistant epilepsy forms.

Biography:

Kuna Yellamma has completed her graduation from Sri Satya Sai Arts & Science College for Women, Anantapur during 1972-75 and Post Graduation in 1977 from S.V.University, Tirupati. She was the recipient of Prof. I.M. Rao Prize for obtaining First Rank in Botany in B.Sc.; secured Second Rank in Zoology in B.Sc. (1975), S. V. University, Tirupati; Fourth Rank in M.Sc. Zoology, S.V.University; Best Speakers prize at seminar in M.Sc. (1977); Commonwealth Academic Staff Fellowship, UK. (1993); S.V.University, Meritorious Women Teacher award-(2000); NTR Mahila Puraskar from Andhra Pradesh State Government, (2001); Honorary Appointment to “The Research Board of Advisors” by American Biographical Institute, USA, (2001-to todate); Nominated for women of the year Award – 2005 by ABI, USA; Shiksha Rattan Puraskar with certificate of Excellence by India International Friendship Society, Bangalore- (2007): S.V.U.Teacher of Excellence Award-2009; NESA Fellowship Award-2010; IAO Certified Faculty Member from International Accreditation Organization, USA– 2012.

Abstract:

Alzheimer\'s disease (AD) is a neurodegenerative disorder mainly occurs in the older people. The pathological hallmark of AD is characterized by the progressive loss of basal forebrain cholinergic neurons that innervate the hippocampus and cortex. Accumulation of extracellular of amyloid-β and intracellular tau protein in brain leads to cognitive impairments. In the present study the rats were injected (I.P.) with D-galactose (D-gal) for 6 consecutive weeks to induced AD characters. The experimental rats were subjected to Morphometric, Learning & Memory efficiency by using Morri water maze test and to investigate neuroprotective activity of the silk Protein, Sericin on Alzheimer’s induced rat. The rats were orally treated with extracted silk protein, Sericin from B. Mori., cocoons. The biochemical changes in Ach and AChE level and Histological pathological changes were observed in selected brain regions. The results of Morphometric, Learning and Memory efficiency, Ach and AChE level and Histological changes revealed that Sericin could reverse the D-Gal induced AD damage in neurons of Cortex and Hippocampus regions and enhances the Learning and Memory efficiency in AD induced rats. From all these findings, it was finally concluded that, Silk Protein, Sericin may be use as a potential cognitive to treat Alzheimer’s Disease.

Biography:

Jack Rogers, PhD. is a Leading authority on the role of RNA in the maintenance of iron homeostasis related to disease processes in the blood (anemia) and in Alzheimer’s disease, and more recently in the etiology of Parkinson’s disease. Director of the Neurochemistry Laboratory in the Psychiatry Department at Massachusetts General Hospital and at the Harvard Medical School, Jack has an extensive funded track record in established scientific journals (Cell, J. Biol. Chem. including cover issue). His peer-reviewed publications won him a Zenith award from the Alzheimer’s Association on the subjects of iron metabolism, and translational control in Neurodegenerative diseases.

Abstract:

Manganese (Mn2+) is an essential trace element although occupational over-exposure to manganese has been linked to a neurodegenerative disease, termed Manganism that is uniquely related, but distinct from Parkinson’s disease. We demonstrated that Mn2+ dose-dependently inhibited translation of both the iron storage protein ferritin and iron-export amyloid precursor protein (APP), each as central iron homeostatic proteins that promote neuroprotective cellular survival in SH-SY5Y neuronal cells, rat brain, and in Parkinson’s disease brain tissue. This action was manifested via iron-responsive element (IRE) sequences in the 5’untranslated region (5’UTR) of the APP transcript. Levels of iron-regulatory protein-2 (IRP-2) translational repressor were decreased in response to Mn2+ influx suggesting that only sufficient levels of IRP1 remained and were therefore critical in the pathway of Mn2+ inhibition of both ferritin and APP translation. Consistently, Mn2+ toxicity was only modestly evident in cells up to 24 hours of exposure, even when these cells progressively exhibited total shut down of the ferritin /APP expression at the level of message translation. In this regard, the consequences of the loss of the protective axis of APP and ferritin expression against iron catalyzed oxidative stress became clear after 24 hours when we observed a consistent and timed dramatic fall in cell viability after 48 hours and 72 hours metal exposure. We conclude the Mn2+ toxicity is partly attributable to translational inhibition pathways operating on APP and ferritin such that their absence embargoes neuroprotective iron export and storage to increase neurotoxic reactive oxygen species (ROS) in these cells, with subsequent and rapid neurotoxicity.