Biography:

Ibtisam Al-Thubaiti has finished his Saudi board in Neurology in 2008. He finished Neuroimmunology fellowship from University of British Colombia in 2011. He is currently a consultant neurologist in King Fahd Specialist Hospital in Saudi Arabia, practicing neurology and neuroimmunology.

Abstract:

Neuromyelitisoptica (NMO) is an inflammatory disease that traditionally described to affect the spinal cord and the eyes causing severe transverse myelitis and optic neuritis. The discovery of disease specific NMO- IgG antibodies in 2004 has revolutionized the understanding of the disease pathology, widened its clinical spectrum, aided in earlier diagnosis, targeted therapy and consequently in a better outcome. Despite that, NMO-IgG antibody sensitivity is high reaching 73% with cell-based assays, there are cases that are seronegative and will be challenging to diagnose. Recently, the discovery of myelin oligodendrocytes glycoprotein (MOG) antibodies in seronegative NMO patients has delineated another spectrum of inflammatory CNS diseases that mimic NMO clinically but not pathologically. This presentation will highlight the clinical picture of NMO spectrum disorder, the diagnostic challenges, 2015 diagnostic criteria, and the differences between anti-NMO and anti-MOG antibody positive disorders. 

Biography:

Ahmed Alhusban graduated from Jordan University of Science and Technology (JUST) in 2008 with a Doctor of Pharmacy (PharmD) degree. He had his PhD in Experimental Therapeutics from University of Georgia, USA. His PhD research was under the supervision of Dr. Susan C. Fagan to study the mechanisms of recovery after cerebral ischemia and how to manipulate them to improve stroke outcome. His PhD thesis focused on interventions to up-regulate brain derived neurotrophic factor (BDNF) mediated signaling after stroke. His research interests are focused on brain angiogenesis. Currently he is an Assistant Professor at the Faculty of Pharmacy, JUST.

Abstract:

Introduction: Angiotensin II type 2 receptor (AT2R) stimulation is neuroprotective after experimental stroke. However, the therapeutic utility of AT2R stimulation has been hampered by the lack of a specific agonist with favorable bioavailability. Compound 21 (C21) - the first non-peptide AT2R agonist - offers a potential option to enhance stroke recovery. This study aimed to investigate the effect of C21 administration on early and late stroke outcomes, and the molecular mediators involved.

Methods: Rats were subjected to 3 h or 90 min of middle cerebral artery occlusion (MCAO) and randomized to intraperitoneal C21 (0.03 mg/kg) or saline at reperfusion. Animals were sacrificed at 24 h or 7 days and brains were collected for molecular analysis and immunostaining, respectively. Functional outcome at days 1, 4 and 7 was assessed blindly. C21 angiogenic potential was assessed in vitro.

Results: After 3 h of MCAO, C21 treatment reduced infarct size and improved behavioral outcome at 24 h without affecting blood pressure. Co-administration of the AT2R antagonist (PD123319) blocked these effects. On the molecular level, C21 decreased brain hemoglobin content, down-regulated apoptotic and oxidative markers, and increased pro-survival molecules in the brain. After 90 min of MCAO, C21 treatment resulted in sustained functional improvement at 7 days, together with increased vascular density in the ischemic penumbra. In vitro, C21 showed a pro-angiogenic effect that was blocked with brain-derived neurotrophic factor neutralization.

Conclusion: These findings demonstrate that a single dose of C21 is neurovascular-protective and improves stroke outcome possibly through increasing neurotrophin activity, mitigating brain inflammation and promoting antioxidant and pro-angiogenic effects.

Biography:

M Sathya is currently working in the Department of Biochemistry at Bharathidasan University in Trichy, India. She has published several original research papers in the reputed journals and participated in the several scientific meetings.

Abstract:

Dysregulation of cholesterol homeostasis has been linked to Alzheimer’s disease (AD) pathology since several decades ago, while the fundamental molecular pathways led by cholesterol and its precursors are still unclear. Amyloid deposition is considered as the principal pathology of Alzheimer’s disease, and the mechanistic link between cholesterol and its intermediates (GGPP and FPP) in amyloid formation has emerged as an unrevealed mystery in the journey of targeting its pathology. Since amyloid precursor protein (APP) is the primary protein involved in the Ab formation, the present study tends to study the role of cholesterol and its intermediates geranyl geranyl pyrophosphate (GGPP) & farnesyl pyrophosphate (FPP) on APP cleavage and processing in CHO-APPswe cell lines. Inhibition of cholesterol biosynthesis not only inhibits the function of cholesterol, but also inhibits the process of prenylation that are the major functions of GGPP and FPP and further it may disturb the cellular homeostasis and are the consequential events that are reported with statin like drugs. Therefore, our study utilized resveratrol (RSV) as a natural polyphenolic compound that is found to exert several neuroprotective functions. Analysis on the therapeutic efficiency of resveratrol (RSV) attenuated cholesterol and isoprenoids mediated alteration in APP cleavage patterns through its ability to promote SIRT1 activity. Further, the APP cleaving enzymes were regulated decreasing total Aβ and Ab42 levels. Therefore, this study provides a therapeutic avenue for use of RSV as a potent drug in regulating vital. 

Biography:

M Sathya is currently working in the Department of Biochemistry at Bharathidasan University in Trichy, India. She has published several original research papers in the reputed journals and participated in the several scientific meetings.

Abstract:

Dysregulation of cholesterol homeostasis has been linked to Alzheimer’s disease (AD) pathology since several decades ago, while the fundamental molecular pathways led by cholesterol and its precursors are still unclear. Amyloid deposition is considered as the principal pathology of Alzheimer’s disease, and the mechanistic link between cholesterol and its intermediates (GGPP and FPP) in amyloid formation has emerged as an unrevealed mystery in the journey of targeting its pathology. Since amyloid precursor protein (APP) is the primary protein involved in the Ab formation, the present study tends to study the role of cholesterol and its intermediates geranyl geranyl pyrophosphate (GGPP) & farnesyl pyrophosphate (FPP) on APP cleavage and processing in CHO-APPswe cell lines. Inhibition of cholesterol biosynthesis not only inhibits the function of cholesterol, but also inhibits the process of prenylation that are the major functions of GGPP and FPP and further it may disturb the cellular homeostasis and are the consequential events that are reported with statin like drugs. Therefore, our study utilized resveratrol (RSV) as a natural polyphenolic compound that is found to exert several neuroprotective functions. Analysis on the therapeutic efficiency of resveratrol (RSV) attenuated cholesterol and isoprenoids mediated alteration in APP cleavage patterns through its ability to promote SIRT1 activity. Further, the APP cleaving enzymes were regulated decreasing total Aβ and Ab42 levels. Therefore, this study provides a therapeutic avenue for use of RSV as a potent drug in regulating vital. 

Biography:

Dmitri A Rusakov is a Professor of Neuroscience and Wellcome Trust Principal Fellow at Institute of Neurology, University College London. His laboratory has been focusing on multi-faceted synaptic mechanisms of memory trace formation in the brain also involving astroglial signaling.

Abstract:

Targeted drug delivery is a high-priority issue in the emerging concept of precision medicine. We have been developing a breakthrough methodology involving nano-engineered biodegradable polymer microcapsules (0.5-2 µm in diameter) that carries medicinal cargo and are equipped with controllable biophysical and cargo-release properties. Our aim has been to implement this technique in the targeted treatment of nervous tissue and potentially other complex tissues. In our recent studies, we have established nano-engineering tools and protocols to encapsulate releasable drugs relevant to neuronal control, with a wide range of parameters that control capsule permeability. In the case study, we used patch-clamp electrophysiology to document physiological effects of encapsulated sodium channel blocker QX-314 on excitability of nerve cells in culture. In experiments on intact animals, we have established beneficial longer-term effects of encapsulated QX-314 injected in vivo, using a standard behavioral model of inflammation-induced peripheral hypersensitivity in the rat. Building upon these advances, we are currently advancing to optimize preparation, delivery and release of encapsulated anesthetics agents, attempting to establish the underlying physiological mechanisms, controlling factors, and a feasible application scope pertinent to this methodology. Our quest should pave the way for exploring future clinical trials involving microencapsulated drug delivery.

Biography:

Mohsin Raza completed his MD and PhD from Pakistan. He completed his post-doctorate from Virginia Commonwealth University in 2000. Dr Raza is basic and clinical neuroscience researcher especially on Epilepsy as well as Multiple Sclerosis and has published his research in famous journals including Brain Research, PNAS, Epilepsy Research, Science and Engineering Ethics and Epilepsy and Behavior. He also teaches Scientific Ethics and is the director of Faculty Development Program at the Faculty of Medicine in his institution and has developed several academic programs for the students and the faculty. 

Abstract:

Proper parental care is an important aspect of the lives of children with epilepsy. The impact of parental education on the Quality of Life (QOL) of these patients is an understudied topic, especially in developing countries. We investigated the QOL and general health (GH) of children with epilepsy presenting at the pediatric neurology clinic at Baqiyatallah Hospital and a private clinic. The QOL in Childhood Epilepsy (QOLCE) questionnaire, that covers physical activity, well-being, cognition, behavior, social activity, overall QOL, and GH, was used for interviewing parents. A total of 106 patients (m=61, 57.5% and f=45, 42.5%; 5–17 years, mean: 10.31±2.91) participated in the study. The maternal education level had a significant impact on the overall QOL (high school: 3.02 ± 0.85 vs. B.Sc.: 3.67 ± 0.61, p b 0.05) and GH (high school: 2.81 ± 0.79 vs. B.Sc.: 3.8 ± 0.94, p b 0.05) of male patients, while paternal education had no significant effect. Multiple linear regression showed that the maternal education level had an independently significant association with the physical activity of the patients (p = 0.02, CI: 1.4–6.25), while the paternal education level had with the well-being (p=0.02, CI: 0.43–5.36). Additionally, the maternal education level (high school vs. B.Sc.) had a significant effect on physical activity, well-being, cognition, and behavior for all of the patients (p<0.05), while the paternal education level had no significant impact. We conclude that maternal education, in particular, plays a significant role in GH and the overall QOL of male patients. 

Biography:

Claire Donnellan is a Registered Psychologist with the Psychological Society of Ireland, and Assistant Professor and Director of International Initiatives with Trinity College Dublin (TCD), Ireland. She graduated with an Honors BSc in Psychology from University of London in 2002 and a PhD in Medical Gerontology from the Department of Clinical Medicine, TCD in 2008. Her work experience in healthcare as a Researcher and Educator expands across the health sciences both here in Ireland and internationally in Australia, United Kingdom and the Middle East. Her research interests include examining the challenges to successful ageing in both healthy ageing and in age-related illness and disease populations; specifically stroke and neurological patient cohorts. She has published widely in neurology, gerontology and psychology journals and her memberships include the International Federation of Ageing, the World Federation for Neuro-Rehabilitation, and both the European and World Stroke Organizations. 

Abstract:

Introduction: The link between psychological comorbidity and biological factors has been well recognized for many conditions; however, less evidence is reported in the context of stroke. The aim of the study was to examine psychological comorbidity and biological correlates post- stroke in a Middle Eastern cohort.

Method: A prospective stroke sample of n=50 patients (case group) and n=50 healthy ageing individuals (control group) were recruited from the largest Medical Complex in Bahrain. A neuropsychological battery of assessments (including global, executive and meta- cognition and mood), were conducted on all participants. Blood samples were taken for ApoE and other biomarkers levels to determine clinical characteristics.

Results: Total metacognition scores were significantly associated with both anxiety (r=.47, p=.001) and depression (r=.54, p<.0001). Global cognition (r=.32, p<.01) but not executive function, was significantly associated with depression only. Metacognition remained a statistically significant correlate with depression (beta=.42, p<.0001) and anxiety (beta=.51, p<.0001) after adjusting for education and global cognition. The most frequent ApoE genotype was É›2/3 in both cases (44%) and control groups (63%). No statistical significant association was found by cognitive impairment stratification and ApoE genotype for either case or control groups. ApoE genotype É›2/4 had worse cognitive function (χ² (3)=8.29, p<.05) in the control group. A statistical significant difference was found between ApoE genotype and total anxiety scores in that ApoE genotype É›3/3 were highly anxious in the case group (χ² (2)=6.77, p<.05).

Discussion: Metacognition is a better determinant of mood symptoms after stroke, especially in regions where illiteracy levels are high in older populations. The presence of ApoE genotype ɛ4/3 and ɛ4/4 was low to non-existent in this sample explaining no significant associations with cognitive impairment. Further examination of mood dysregulation and ApoE genotype polymorphism may be warranted post-stroke.