Biography:

Khin Maung Bo is involved in neurorehabilitation for over 20 years. He is a Lecturer (Hon) in Hull York Medical School teaching 4th year medical students in CNS and musculoskeletal blocks. He is doing botulinum toxin injection in spasticity, dystonia and involuntary movement disorders for over 15 years and has done poster and oral presentations in international neurorehabilitation conferences. He is also involved in using functional electrical stimulation (FES) over 10 years and presented regularly in international FES conferences. He is working on developing hypertonic hand monitoring scale.

Abstract:

Demyelination affects highly myelinated structures like corpus callosum (CC). CC is unique in function that it connects right and left hemisphere and it synchronises bimanual or bipedal activities. Affecting CC can disturb synchrony between the two hemispheres and will affect bimanual and bipedal tasks. The aim is to see if speed of clapping (bimanual activity) can reflect the involvement of CC in multiple sclerosis. Consecutive 70 multiple sclerosis patients from outpatient clinics and home visits were tests for bimanual hand function (clapping). Exclusion criteria are upper limb power <3/5 MRC scale, pain, visual impairment, intentional tremors, stroke or cognitive impairment. Study period started from 01.09.2016. Comparison of speed between rapid supination/pronation of left and right hand separately and then clapping of both hands (supination/pronation of each hands alternatively) were conducted. Patients had to do as fast as they could and noticeable slowing of clapping comparing to single hand supination/pronation was taken as a sign slowing down of conduction through CC. 31 patients were excluded, 34 patients showed no noticeable difference, 2 patients were difficult to make conclusions and 3 patients showed definite slowing down in clapping. Positive patients will have difficulties in doing bimanual activities like using two sticks for mobility, typing using keyboard, pushing wheel chair bimanually etc. It is possible to detect CC involvement by doing above bedside test and can be used in rehabilitation setting. Sample size is not large enough and larger studies need to follow to validate the finding.

Biography:

Gary Sinoff is a geriatrician with expertise in psychogeriatrics. He is Clinical Assistant Professor in the Faculty of Medicine, Technion- Israel’s Institute of Technology and senior lecturer in the Department of Gerontology, Faculty of Social Welfare and Health Studies, University of Haifa. His research and teaching are in the areas of geriatric assessment, cognitive impairment, anxiety, depression, research ethics, and death anxiety. He has published, and presented his research both locally and internationally. He is involved in educating students of gerontology, physicians, nursing students, occupational therapists and administrative directors of long-term care institutes. The impact of his work has been recognized both locally and internationally.

Abstract:

Anxiety as a separate disorder was reintroduced into the DSM manuals in 1980 but is now widely recognized as probably the most common mood disorder in the elderly, with a prevalence ranging between 10% to 20%, greater than for depression. The elderly may not meet the full requirements for an anxiety disorder, yet they still experience enough symptoms which can disrupt their daily lives. During the last years, the interaction between neuropsychiatric syndromes and cognition has been widely researched in view of the fact that these symptoms have been reported to accompany memory loss especially in the initial stages of cognitive decline. In fact, anxiety/depression have been reported to not only be a reaction to cognitive decline, but also possible predictors of future cognitive decline. The debate is intensified by studies showing that anxiety and not only cognitive decline have shown an increase in Aβ in the amygdala as well as in the hippocampus. Since cognitive decline now has become a major burden to society, if one could delay the decline by initiating treatment as early as possible, the savings, for both the individual and society, would be significant. Some studies have shown that anxiety is more prevalent in early mild cognitive impairment and subjective cognitive impairment, and may have a predictive value for the future cognitive decline, but the predictive value in the late mild cognitive impairment is still debatable. Anxiety is inter-related and inseparable with loss of memory and has sometimes been shown to be a predictor for the future cognitive decline, shown in studies published by some years ago. Theoretically, this may be explained by Braak and Braak’s staging with changes initially in the entorhinal cortex, spreading to the hippocampus and amygdala and finally to the cortex. This lecture will relate to anxiety in the elderly, its high prevalence, the problems in its detection and especially its interaction with cognitive decline.

Biography:

Ghazi Daradkeh is a clinical dietitian supervisor in Nutrition & Dietetics department - Al Khor Hospital – Hamad Medical Corporation – Qatar and clinical preceptor of human nutrition program at Qatar University ACEND. He completed his Ph.D. in clinical nutrition and dietetics specifically in traumatic brain injury nutritional status at sultan Qaboos University, Oman, in October 2016. He received his Master’s degree in maternal and child nutrition from faculty of medicine-public health department at Jordan University of Science and Technology Jordan, in 1995 and his Bachelor degree in human nutrition from same university, in 1990. He is a reviewer and editorial board member of the International Journal of Nutrition, Pharmacology, Neurological Diseases (USA), reviewer for British Journal of Medicine and Medical Research (UK) and a member of an International Neuro Society (INS), Australia, Linnaean Society (FLS) UK, and International Society of Antioxidants in Nutrition & Health (INSAH), Diabetes Association (QDA), Qatar and Environmental Friend Center (QEFC), Qatar.

Abstract:

Objective: The aim of this study were to assess the nutritional status and macronutrients adequacy of traumatic brain injury (TBI) patients and controls, attending treatment from a specialized unit in Qatar.

Research Design and Methods: This study was conducted among male (TBI) in-patients admitted in Rumailah Hospital Rehabilitation Unit, Hamad Medical Corporation-Doha, Qatar from August 2014 to June 2015 (21 cases and 21 healthy volunteers). The attendees were consecutive patients with TBI. Demographic variables were solicited via medical records or directly from the attendees with TBI. Anthropometric measurements and dietary intake (24- hour recall) were collected and assessed by the super tracker.

Results: Half of the participants (52.4%) were of age 30 -38 years range. Approximately 23.8% of cases were classified as having ‘mild TBI’ while 28.6% and 47.6% were classified as moderate and severe TBI respectively. In terms of nutritional parameters, three fourth (76.2%) of the cases were at high or moderate risk of malnutrition, 23.8% of cases were underweight, while 66.7% in the normal range and 9.5% were overweight. TBI patients were noted to have a deficiency in energy (30.2%), carbohydrate (43.0%), protein (24.8%), and fiber (54.1%) intake.

Conclusion: Despite the high prevalence of TBI in emerging economies such as Qatar, to our knowledge, there is a dearth of studies examining the nutritional status and its correlates among the TBI population. This study indicates that TBI patients in Qatar are at a high risk of developing malnutrition, and macronutrients deficiency. Therefore, nutritional assessment, intervention, and support are highly essential to improve TBI patient’s health status beyond the brain injury.

Biography:

Abstract:

Biography:

Maria Silvia Lopez Alonso is a Pre-doctoral researcher at the UCV, 3rd year. Thesis title is Study of Valencia for the practice of Physical Education of the Elderly according to the Vancouver Protocol and obtained Degree in Religious Sciences UCV, Master in Marriage and Family UNAV1, Master’s Degree Education and Rehabilitation of Addictive Behaviors UCV, 2nd course in Psychology at the UCV. Own trademark: “Active Aging for 50 by Silvia López”.

Abstract:

The following study aims to publicise the neurological research work of Jordi Cervós Navarro through some of his conferences, speeches and talks.When Jordi Cervós Navarro - born in Barcelona (Spain) in 1930 - finished his degree in medicine, (1952) he travelled to Austria and Germany to work as a doctor in neurology clinics. Since 1954 he has been an associate lecturer and since 1961, a lecturer in neuropathology at the Free University of Berlin (Germany). From 1968 until 1998 he was a professor of neuropathology at this same university. Cervós, when embarking on his career in Austria, devoted himself to psychiatry, but over time he edged towards neuropathology. As a neurologist, his studies focused on the Metabolic and Degenerative Diseases of the Central Nervous System, of the Cerebellum, Brain Stem, and Spinal Cord (Spinocerebellar Degenerations), disorders of Lipid, Pigment, Protein or Mineral Metabolism or blood-Spinal Cord and Brain Barriers in Health and Disease for example. Cervós has had a prolific career of research and exhibition of his works that has taken him around the world for almost 50 years.

Biography:

Mzia Zhvania is a Doctor of Science, Professor at Ilia State University and head of the Department of Brain Ultrastructure and Nanoarchitecture, I. Beritashvii Center of Experimental Biomedicine, Tbilisi, Georgia. She is an author of more than 80 scientific articles, published in reputed journals and the participant of numerous international scientific conferences. Mzia Zhvania permanently organizes international scientific mini-symposiums, concerning different aspects of neuroplasticity, Mzia Zhvania is a board member of two international scientific journals.

Abstract:

The ability of chronic motor deficit to produce alterations on the functioning of the central nervous system has been studied extensively. However, many questions still demand further investigation. Thus, the consequences of such limitation on the brain structure have been described only in a few studies. Moreover, the biggest part of research has been focused on restraint stress, while the effect of mild motor deficit are not well elucidated. In the present comparative electron microscopic study, we examine the effects of 40-day restraint stress and moderate motor deficit on the ultrastructure of limbic, extrapyramidal and neocortical regions of rat brain – the central and lateral nuclei of amygdale, the CA and CA3 hippocampal areas, caudate nucleus and neocortical motor area. Both types of motor deficit produce ultrastructural modifications, however the effects of diverse motor experiences are not the same. Chronic restraint stress produces much more significant pathologies, which are mainly concentrated in the central amygdale nucleus – brain region, which is actively involved in the organization of stress-response. Mild motor deficit produces mainly moderate modifications. They are concentrated mostly in the caudate nucleus, which is actively participates in motor and cognitive functions. In both cases the motor cortex retains almost normal ultrastructure. Therefore, we suggest that chronic motor deficit itself does not alter significantly the architecture of brain. More substantial modifications should produce stress, which often accompanies some forms of motor deficit.

Biography:

Fiorenza Stagni obtained her PhD in Biomedical Sciences at University of Bologna, Italy in 2014. She is currently involved as Postdoctoral fellow in an international project aimed at identifying a panel of drugs that may be safely used during pregnancy or in infants in order to counteract the neurodevelopmental defects linked to Down syndrome. In 2016, she was awarded by the Trisomy 21 Research Society for the Best Dissertation in the field of DS defended in 2014-2015. She has published more than 15 papers in the field of preclinical studies for the treatment of cognitive deficits in DS.

Abstract:

No therapies currently exist for intellectual disability in Down syndrome (DS), a relatively high-incidence genetic condition (1:700/1000). Neurogenesis impairment starting from fetal life stages is considered a major determinant of intellectual disability in DS. We have previously shown that perinatal treatment with fluoxetine, an antidepressant, fully restores neurogenesis and cognitive performance in the Ts65Dn mouse model of DS. The finding that these effects were accompanied by an increase in the levels of brain-derived neurotrophic factor (BDNF) suggests that BDNF may be an important determinant of the proneurogenic effect of fluoxetine. This important discovery prompted us to find a therapy that is as effective as fluoxetine but that may pose fewer caveats for clinical application in children with DS. A therapy based on BDNF is impracticable due to its poor blood-brain barrier penetration. However, the naturally-occurring flavone 7,8-DHF is a BDNF mimetic that crosses the blood-brain barrier and binds to the BDNF TrkB receptor. Based on these premises, the goal of our study was to establish whether early treatment with 7,8-DHF can rescue trisomy-linked neurodevelopmental defects, similarly to fluoxetine. We found that neonatal treatment with 7,8-DHF increased neurogenesis and restored neuron maturation in the hippocampus of Ts65Dn mice. Importantly, Ts65Dn mice treated from birth to adolescence exhibited restoration of hippocampus-dependent memory. This study provides novel evidence that treatment with a natural compound 7,8-DHF restores brain development and cognitive performance in a DS mouse model. In view of the safe nature of 7,8-DHF our results, potentially, are readily transferable into clinical practice.

Biography:

Farnaz Nikbakht was born in Tehran, Iran, on 8 October 1969. Before obtaining her Ph.D. degree in Human Physiology from Shiraz University in 2007, she received an award from the Iran Ministry of Health and Education and spent six months at Flinders University, Adelaide, Australia for completing her research on degenerative diseases. Now, as the Associate professor of Department of Physiology, in Iran University of Medical Sciences, she has managed several research programs and has conducted the thesis of several Masters and Ph.D. students in her Lab. Since 2010 she has directed a research team on Epilepsy and Alzheimer’s diseases fields in her lab. Her research leads to publishing several articles.

Abstract:

Background & Purpose: Apigenin, a non-toxic and non-mutagenic flavone, has the potential of free radical scavenging activity. Recent studies revealed the protective effect of apigenin against Aβ neurotoxicity but the underlying mechanism was unclear. The purpose of this study was to reveal the protective effect of apigenin against Aβ 25-35 by inhibition of mitochondrial caspase 9 and cytochrome C release. The ability of apigenin to prevent dynamin-related protein (Drp1) activation and thereby protection against mitochondrial fragmentation and dysfunction was the second goal of this study.

Methods: Aβ 25-35 was microinjected into the left lateral cerebral ventricle. Oral administration of apigenin was started half an hour before the surgery and continued for the following 21 days. After three weeks, the animals were sacrificed and their brains were removed for further histological and molecular processes. Cell death and neurodegeneration was assessed by Nissl and Fluoro Jade B staining in CA1 area of the hippocampus. Cytochrome C and caspase 9 was detected by immunohistochemistry in the same area and Drp1 was detected by western blotting.

Results: The results revealed that oral administration of apigenin protected CA1 neurons from Aβ toxicity (P<0.001 for Nissl and Fluoro Jade B). The protection was associated with a significant decrease in mitochondrial caspase 9 and Cytochrome C release (P<0.01). Drp1 was also significantly decreased in apigenin treated groups (P<0.01).

Conclusion: These data demonstrate that the flavone apigenin protects highly vulnerable CA1 neurons against Aβ toxicity and suggest that it is mediated by amelioration in mitochondrial dysfunction.