28^th World Summit on Neurology, Neuroscience and Neuropharmacology September 26-27, 2018 Montreal, Quebec, Canada

Biography:

Dr. Peijun Li received his PhD from Department of Physiology and Biophysics, Georgetown University Medical Center. His research during his PhD study has been focusing on the inhibitory interneurons in mouse somatosensory cortex. During his postdoctorial work at Children’s National Medical Center at DC, he studied how hypoxia could affect the brain development using mouse model, and also how disruption in circadian gene expression could result in epilepsy in both human and mouse model. Dr. Li is now a principle investigator at Second Affiliated Hospital, Wenzhou Medical University, China. As a scientist with expertise in electrophysiology, his work will be directed towards understanding the functional roles of specialized GABAergic inhibitory circuits in the pathophysiological process of epilepsy and circuit formation. In his free time, Dr. Li likes running and listening to music. He have finished four half marathons and three full marathons which include the Marine Corps Marathon 2016 and the Rock and Roll DC 2016, His personal best is 3:53:25. 

Abstract:

Because molecular mechanisms underlying refractory focal epilepsy are poorly defined, we performed transcriptome analysis on human epileptogenic tissue. Compared with controls, expression of Circadian Locomotor Output Cycles Kaput (CLOCK) is decreased in epileptogenic tissue. To define the function of CLOCK we generated and tested the Emx-Cre; Clock^flox/flox and PV-Cre; Clock^flox/flox mouse lines with targeted deletions of the Clock gene in excitatory and parvalbumin (PV)-expressing inhibitory neurons, respectively. The Emx-Cre; Clock^flox/flox mouse line alone has decreased seizure thresholds, but no laminar or dendritic defects in the cortex. However, excitatory neurons from the Emx-Cre; Clock^flox/flox mouse have spontaneous epileptiform discharges. Both neurons from Emx-Cre; Clock^flox/flox mouse and human epileptogenic tissue exhibit decreased spontaneous inhibitory post-synaptic currents. Finally, video-EEG of Emx-Cre; Clock^flox/flox mice reveals epileptiform discharges during sleep and also seizures arising from sleep.  Altogether, these data show disruption of CLOCK alters cortical circuits and may lead to generation of focal epilepsy, which suggest that the circadian pathway may be a promising target for therapeutic intervention.

Biography:

Dr. MARCIO ROBERTTI RAMALHO DA CUNHA is senior instructor at The Clinic Trauma Centre at Brazil. He completed this medical schooling from Federal University of Rio Grande Do Norte in 1983 – 1989. After completing his medical schooling he worked as Medical Residence at Base hospital Brazil in year 1990 to 1993. He complete post-graduation course from R.W.T.H Hospital, Aachen-Germany( 1994) and Freie University,Berlim, Germany(1997).

He is titular member of Brazilian  Neurosurgery Society (1994), Brazilian Spine Society (2009), Brazilian M.I.S Society (2012) and Latino American Study Group Of Neuroendoscopy / Glen (2016).

He holded the position of U.F.R.N, Assistant Professor Of The Neurosurgery Department ( 1996-1999 ),

Senior Staff Of The Spinal Surgery Area Of Clinic Trauma Center /Natal-Rn (2007), Chairman Of Neurosurgery Service Of The General Hospital / Natal-Rn (2014) and Coordinator Of The Spinal Endoscopy  Surgery Field -  Ab Health Institute  (2016)

Abstract:

We have a lot of causes to entrap the lumbar nerve roots, bringing sciatica as a major symptoms, these entrapments can be a  result from many etiologies such as intervertebral disc herniation , spinal stenosis , the formation of osteophytes and the fibrous adhesive entrapment (     ).We present a A 58-year-old woman presented to our clinic in march 2017, complaining of severe right sciatica her complains were aggravated by walking and coughing and prolonged sitting position, she was also experienced numbness and a tingling sensation in the lateral portion of her right foot .On physical examination the straight leg raise test was positive only in her right side ,with a 45 angle raise, her Achilles tendom reflexe was abolished . The Lumbar MRI showed no remarkable signs of nerve block in the level L5/S1 to explain the origin of the pain .  We've made a nerve root block using 01 cc of  lidocaine of the right S1 root with complete relief of the symptoms for eight hours . In face a positive result of the blockage  test, we´ve done a full endoscopy interlaminar approach .We've made the procedure under the steps of the full endoscopic interlaminar approach by Rueten technical (    ). After open the yellow flavum ligament we could see a total S1 root entrapment by fibrous adhesive tissue with no signs of the S1 root ,after some manipulations we could see how entrapted was the nerve root with some  surgical manueveres using the disector and scissor punch , we could liberate the nerve root until its entrance in the foramen .The procedure took around 34 minutes with a patient hospital discharge around six hours, using a single pain killer to control the lumbar back pain in the first 24 hours .

Biography:

Seyed Behnamedin Jameie is the Director of Neuroscience Research Center of Iran University of Medical Sciences at the level of Full Professor of Anatomy and Neuroscience. He has published more than 70 papers in reputed journals and has been serving as an Chief Editor of Thrita Journal.    
 

Abstract:

Spinal cord injury is suffering medical condition that might happen to anyone. Therapy mainly focuses on rehabilitation and pharmacological treatment. Supra-spinal changes in cerebellum that receives afferents from spinal cord might be the reason of unsuccessful therapy. The expression of FNDC5 was reported in cerebellar Purkinje cells. In the present study, we considered the expression of FNDC5 in Purkinje cells following SCI with and without MP administration in adult rat with SCI. Thirty-five adult male rats were used. The animals randomly allocated in five groups, including SCI, spinal cord injury with methylprednisolone treatment, operation sham, control and operation sham with MP. SCI was done by using special clip to compress the spinal cord at supposed level. Then the animals went under study for FNDC5 expression, apoptosis by using immunohistochemistry, western blotting, TUNEL and Nissl staining. Our results showed significant decrease in the number of Purkinje cells following SCI. Therapy with MP inhibits the apoptosis in irFNDC5 Purkinje cells and restore them. Expression of FNDC5 significantly increased in SCI and decreased following MP therapy. We also showed other cerebellar cells with FNDC5 immunoreactivity in the two other cerebellar layers that is firstly reported. Since the irisin is known as the plasma product of FNDC5 we think that it might be a plasma marker following therapeutic efforts of SCI, however it needs further research. In addition it is possible that changes in FNDC5 expression in purkinje cells might be related to neurogenesis in cerebellum with unknown mechanisms

Biography:

Dr. Namrata Singh received her Ph. D degree from Pt. Ravishankar Shukla University, Raipur, India, in 2013 in physico-organic chemistry with Prof. Kallol K. Ghosh. Her thesis research interests were surfactants, micellar kinetics and oxime based AChE reactivators. She worked for two years as postdoctoral-scientist with Prof. ZdenÄ›k Fišar at first faculty of medicine, Charles University in Prague, Czech Republic and studied the genetic, biological and environmental factors of mental disorders especially cognitive enhancers and mitochondrial functions. In 2015 she joined Department of chemistry, Indian Institute of Technology, Bombay as postdoctoral fellow to study drug-protein interactions and their biothermodynamics. She is currently working as Assistant Professor at Department of Engineering Sciences, DY Patil’s Ramrao Adik Institute of Technology, Mumbai. Her current research interests include neurodegenerative disorders particularly Alzheimer’s disease, cannabinoids and mitochondrial respiration, cholinesterase inhibitors, bio-thermodynamics of drug-protein, drug-surfactant and drug-drug interactions. She has published seventeen research articles, one short communication, one book chapter and four review articles in journals of high repute. She has bagged prestigious scientific awards and recognitions including Young Scientist Awards and national and international research fellowships. She is interested in physicochemical and biochemical aspects of drugs for neurodegenerative disorders. Currently her research interests include drug-protein interactions and aggregation/fibrillation of proteins.

Abstract:

Statement of the Problem: The pharmacokinetics and pharmacodynamics of a drug can be well understood and interpreted by measuring the extent of drug binding to plasma proteins.  Reliability of a protein-protein interaction model specific to Alzheimer’s disease (AD), can lead to screening, and prioritization of novel protein candidates [1]. Thus, the investigation of such molecules with respect to albumin binding is of imperative and fundamental significance. Methodology & Theoretical Orientation: Spectroscopic (UV-Visible absorption, steady-state fluorescence and circular dichroism) and calorimetric (isothermal titration calorimetry) techniques have been employed to investigate the interactions of water soluble novel Novel Alzheimer’s drug candidates (7-MEOTA-donepezil like compounds) with bovine serum albumins (BSA) under physiological conditions. Fluorescence quenching spectra in combination with circular dichroism (CD) spectroscopy was used to investigate the drug-binding mode, the binding constant and the protein structure changes. The apparent binding constants and number of substantive binding sites using site markers (warfarin and diazepam) have been evaluated by fluorescence quenching method. The thermal unfolding of BSA in absence and presence of drugs has been studied by CD spectroscopy. Findings: The drugs substantially quenched the intrinsic fluorescence of BSA. Synchronous fluorescence studies indicate the binding of selected Alzheimer’s drugs with BSA mostly changes the polarity around tryptophan residues rather than tyrosine residues. The circular dichroism studies indicate that the binding has induced considerable amount of conformational changes in the protein. However, calorimetric studies did not manifest drug-protein binding. Conclusion & Significance: Binding of the selected Alzheimer’s drug revealed static quenching mechanism through hydrogen bonds and van der Waal’s attraction. The thermodynamic parameters indicated that hydrophobic and electrostatic interaction played main role in the binding. An understanding of detailed energetic and mechanism of binding may be useful for providing safer and efficient therapies for Alzheimer’s disease and diagnoses in clinical settings as well [2]. A systematic review of attempts and achievements of such interactions has been done and future scope has been predicted. Outcomes for therapy with AD drugs already under clinical trials have been studied carefully and discussed. 

Biography:

Hamdallah Delaviz completed his Ph.D. at Tehran Medical University, Iran, in Anatomy. He is currently the deputy of Medical School, Yasuj University of Medical Sciences. He is a Fellow of the Iranian Society Anatomical Sciences and Physiotherapy Association. He is pursuing a career in spinal cord injury

Abstract:

Background; The WHO disclosed that 50.1% of consumptions worldwide belong to spirits, with adolescents having the highest proportions of drinkers in Europe and the Americas, along with prevalent monthly heavy episodic drinking. Alcohol abuse has substantial health consequences, especially in adolescence, considered to extend from 12 to 25 years [1]. Importantly, adolescent and adult brains are different in their responses to alcohol consumption, particularly ethanol [2]. Indeed, the adolescent brain undergoes maturation through structural and functional changes [3]. However, consumption of alcoholic drinks containing methanol increased in the last years due to the production of counterfeit or local spirit drinks. Most therapies for alcoholism contain side effects while some are even toxic and invasive. [4-7] Material and methods; In this study, we investigated the effects of methanol administration on memory function and pathological outcomes in adolescent rats, focusing on the hippocampus and explored the efficacy of Light-Emitting Diode (LED) therapy in this model. Results; Results of behavioral tests showed that LED therapy significantly improved memory impairment resulted by acute and chronic methanol administration at 7 and 28 days, respectively. Immunohistochemical staining demonstrated hippocampus damage and cell edema in methanol rats, compared to controls, as measured by increased apoptosis (caspase-3+ cells), whereas LED therapy significantly decreased these outcomes. In contrast, LED therapy significantly increased the proliferation rate as measured by Ki-67. On the other hand, the number of GFPA and BDNF+ cells in the hippocampus and the serum level of BDNF significantly decreased in methanol group, compared to controls, however, LED therapy reverted these values to normal. Although chronic administration of methanol (28 days) led to severe pathological situations, compared to acute (7 days), however, short- and long-term LED therapy was efficient. Conclusion; In conclusion, we showed that chronic methanol administration caused severe memory impairments which could be improved by LED therapy. Results of our study favor the interaction between BDNF and astrocytes against methanol-induced neurotoxicity. Finally, LED efficiently improved the memory function and recovered the pathological situation resulted by methanol consumption, which makes it as a potent candidate in alcoholism treatment. Further studies are needed to explore the mechanisms responsible for secretion of BDNF by astrocytes and the improvement by LED phototherapy in the brain, especially in different areas of the hippocampus. 

Biography:

Taraneh Bahremand has completed his PharmD. at the age of 24 years from Tehran University of Medical Sciences and master of health profession education(MHPE) and public health (MPH) studies from Tehran University of Medical Sciences . She is the medical advisor of supplement drugs in OrchidPharmed Co., a pharmaceutical marketing company. She has published 4 papers in reputed journals.

Abstract:

Licofelone is a dual COX/5-LOX inhibitor which is approved as a potential treatment for osteoarthritis. Its anti-inflammatory and analgesic properties have been shown before. Besides, recent studies identified neuroprotective and anti-oxidative roles where oxidative stress underlies Central Nervous System disorders. The anti-seizure activity was demonstrated in several animal models of epilepsy. Seeking underlying mechanisms for central effects of this drug, researchers have suggested various neurotransmitters and neuro-modulators as likely targets of licofelone. The involvement of nitric oxide synthase (NOS) in anti-seizure mechanisms of licofelone is addressed recently. In the present behavioral investigation, we utilized pentylenetetrazole-induced clonic seizure model to seek consequences of licofelone administration. We investigated the role of NMDA in the anticonvulsant effect of Licofelone in the pentylenetetrazole (PTZ)-induced seizure in mice.  Licofelone revealed anticonvulsant properties at the dose of 10 mg/kg (i.p) or higher in mice. MK801, a selective NMDA antagonist, significantly enhanced this anticonvulsant effects in combination with sub-effective dose (5mg/kg) of licofelone.

On the other hand, pre-treatment with selective NMDA agonist (D-Serine) reversed the anticonvulsant effects of licofelone. This data implies that antagonizing of NMDA receptors seems crucial for anticonvulsant properties of this COX/5- LOX inhibitor in seizure susceptibility. Our findings point to the involvement of NMDA as an essential role player in the central neuro-protective properties of licofelone.

Biography:

Taraneh Bahremand has completed his PharmD. at the age of 24 years from Tehran University of Medical Sciences and master of health profession education(MHPE) and public health (MPH) studies from Tehran University of Medical Sciences . She is the medical advisor of supplement drugs in OrchidPharmed Co., a pharmaceutical marketing company. She has published 4 papers in reputed journals.

Abstract:

Licofelone is a dual COX/5-LOX inhibitor which is approved as a potential treatment for osteoarthritis. Its anti-inflammatory and analgesic properties have been shown before. Besides, recent studies identified neuroprotective and anti-oxidative roles where oxidative stress underlies Central Nervous System disorders. The anti-seizure activity was demonstrated in several animal models of epilepsy. Seeking underlying mechanisms for central effects of this drug, researchers have suggested various neurotransmitters and neuro-modulators as likely targets of licofelone. The involvement of nitric oxide synthase (NOS) in anti-seizure mechanisms of licofelone is addressed recently. In the present behavioral investigation, we utilized pentylenetetrazole-induced clonic seizure model to seek consequences of licofelone administration. We investigated the role of NMDA in the anticonvulsant effect of Licofelone in the pentylenetetrazole (PTZ)-induced seizure in mice.  Licofelone revealed anticonvulsant properties at the dose of 10 mg/kg (i.p) or higher in mice. MK801, a selective NMDA antagonist, significantly enhanced this anticonvulsant effects in combination with sub-effective dose (5mg/kg) of licofelone.

On the other hand, pre-treatment with selective NMDA agonist (D-Serine) reversed the anticonvulsant effects of licofelone. This data implies that antagonizing of NMDA receptors seems crucial for anticonvulsant properties of this COX/5- LOX inhibitor in seizure susceptibility. Our findings point to the involvement of NMDA as an essential role player in the central neuro-protective properties of licofelone.