Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 9th International Conference on Brain Disorders and Therapeutics Paris, France.

Day 1 :

  • Brain Disorders | Brain Cancer & Tumors | Neurological Disorders | Neuroimmunology | Neurosurgery | Traumatic Brain Injury | Mental Retardation | Neuroinflammation | Pathophysiology of Brain Disorders | Cerebrospinal Complications | Brain Complications | Neurodegeneration & Aging Disorders | Pediatric Neurology | Neuropharmacology | Neurology of Brain | Novel Treatment Strategies | Addiction & Brain Disorders | Analysis, Assessment and Diagnosis of Brain Disorders | Stem Cell Therapies | Neuro Oncology
Location: Webinar

Session Introduction

Maryam Bazrgar

Damghan University, Iran

Title: Melatonin Ameliorates Oxidative Damage Induced by Maternal Lead Exposure in Rat Pups

Time : 09:00-9:40

Speaker
Biography:

I am physiologist and now I am a PhD candidate of neuroscience at the age of 33 from the Neuroscience Research Center, Shahid Beheshti University of Medical Science, Tehran, Iran.

Abstract:

During the particular period of cerebellum development, exposure to lead (Pb) decreases cerebellum growth and can result in selective loss of neurons. The detection and prevention of Pb toxicity is a major international public health priorities. This research study was conducted to evaluate the effects of melatonin, an effective antioxidant and free radical scavenger, on Pb induced neurotoxicity and oxidative stress in the cerebellum. Pb exposure was initiated on gestation day 5 with the addition of daily doses of 0.2% lead acetate to distilled drinking water and Continues until weaning. Melatonin (10mg/kg) was given once daily at the same time. 21 days after birth, several antioxidant enzyme activities including superoxide dismutase (SOD) and glutathione peroxidase (GPx) were assayed. Thiobarbituric acid reactive substance (TBARS) levels were measured as a marker of lipid peroxidation. Rotarod and locomotor activity tests were performed on postnatal days (PDs) 31–33 and a histological study was performed after completion of behavioral measurements on PD 33. The results of the present work demonstrated that Pb could induce lipid peroxidation, increase TBARS levels and decrease GPx and SOD activities in the rat cerebellum. We also observed that Pb impaired performance on the rotarod and locomotor activities of rats. However, treatment with melatonin significantly attenuated themotoric impairment and lipid peroxidation process and restored the levels of antioxidants. Histological analysis indicated that Pb could decrease Purkinje cell count and melatonin prevented this toxic effect. These results suggest that treatment with melatonin can improve motor deficits and oxidative stress by protecting the cerebellum against Pb toxicity.

Speaker
Biography:

Dr. Albay is currently a 2nd year medical resident in Cardinal Santos Medical Center. She has earned her Doctor of Medicine Degree from the University of the Philippines, Manila and her Bachelor of Science in Chemistry from the University of the Philippines Diliman, graduating Magna Cum Laude. To date, researches conducted by Dr. Albay have been included in oral presentations in local symposiums such as the Philippine Chemistry Congress, Joint Conference of 2012 Asia Pacific Conference on Analytical science and 3rd Regional Electrochemistry Meeting of Southeast Asia last 2012.

Abstract:

New evidence on the efficacy and safety of dual antiplatelet therapy for secondary stroke prevention have been realized in the recent years. An updated meta analysis was done to determine the effect of the various dual antiplatelets (including ticagrelor and cilostazol) vs aspirin alone on recurrence rate of ischemic stroke, cardiovascular morbidity and mortality, and its safety profile as reported through major bleeding.

Pariya Khodabakhsh

Shahid Beheshti University of Medical Sciences, Iran

Title: The Effect of Insulin on Schwann Cell Differentiation of Rat Epidermal Neural Crest Stem Cells

Time : 10:20-11:00

Speaker
Biography:

Pariya Khodabakhsh has completed her doctorate in pharmacy at the age of 25 years from Islamic Azad University of Pharmaceutical Sciences in 2014. She is a fifth-year Ph.D candidate in pharmacology at  Shahid Beheshti University of Medical Sciences. She has authored numerous papers in national and international journals and conferences. Her current areas of research interest include neurodegenerative diseases, regenerative medicines and neuropharmacology.

Abstract:

Schwann cells (SCs) play a crucial role in successful nerve repair and regeneration in both the peripheral and central nervous systems and promise to be a useful tool for cell-based therapies, disease modelling and drug discovery. Therefore, establishment of a procedure to obtain activated, highly proliferative SCs, in an appropriate time for clinical applications, is a prerequisite. However, the sources of SCs are limited both for studies of SC development and biology and for the development of treatments for SC-associated diseases. It is previously showed that epidermal neural crest stem cells (EPI-NCSCs) are a biologically relevant source for generating large and highly pure populations of SCs. Insulin is a peptide growth factor that regulates the transport, synthesis and storage of substances required for growth and differentiation of various kinds of developing cells. Regarding to the role of insulin in myelinating SC differentiation, in present study, we aim to examine the impact of insulin, on the cell viability and SC differentiation of EPI-NCSCs, isolated from bulge of rat hair follicles, through MTT and real-time quantitative PCR analysis, respectively.  Insulin treatment at concentrations of 0.005-5 µg/ml increased the cell viability, dose dependently. Insulin exposure (5 µg/ml) increased gene expression of BDNF, FGF2 and IL-6 in EPI-NCSCs from day 1 to 6, while EGR1 (as a non-myelinating SC marker) was downregulated. Taken together, these results may corroborate the critical importance of insulin in pursuit of SCs through induction of SC differentiation of EPI-NCSCs.

Speaker
Biography:

I am studying PhD at Shahid Beheshti Neuroscience Research Center. So far I have published two papers on physiology and behavior.

Abstract:

Melatonin is a radical scavenger with the ability to remove reactive oxidant species. There is report that coexposure to lead and ethanol during developmental stages induces learning and memory deficits and oxidative stress. Here, we studied the effect of melatonin, with strong antioxidant properties, on memory deficits induced by lead and ethanol co-exposure and oxidative stress in hippocampus. Pregnant rats in lead and ethanol coexposure group received lead acetate of 0.2% in distilled drinking water and ethanol (4 g/kg) by oral gavages once daily from the 5th day of gestation until weaning. Rats received 10 mg/kg melatonin by oral gavages. On postnatal days (PD) 30, rats trained with six trials per day for 6 consecutive days in the water maze. On day 37, a probe testwas done and oxidative stress markers in the hippocampus were evaluated. Results demonstrated lead and ethanol co- exposed rats exhibited higher escape latency during training trials and reduced time spent in target quadrant, higher escape location latency in probe trial test and had significantly higher malondialdehyde (MDA) levels, significantly lower superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities in the hippocampus. Melatonin treatment could improve memory deficits, antioxidants activity and reduced MDA levels in the hippocampus. We conclude, co-exposure to lead and ethanol impair memory and melatonin can prevent from it by oxidative stress modulation.

Fatemeh Mahboobifard

Shahid Beheshti University of Medical Sciences, Iran

Title: Sex-related Differences in Estrogen Receptors and Tumor Proliferation Factors in Macroprolactinomas

Time : 11:40-12:20

Speaker
Biography:

Fatemeh has completed her Pharm.D at age 25 years and worked as a pharmacist for 9 years. Then she started studying pharmacology at PhD degree in Shahid Beheshti University. She achieved 1st  rank among Shahid Beheshti university students at Entrance Exam of Pharmacology and Board Comprehensive Exam of Pharmacology. Her PhD GPA is 18.75. She is considered a talented student at university. She has published 4 papers, the most recent of which has been published in the official journal of pituitary society in 2020. She has been serving as a reviewer board member of the journal “Physiology and Pharmacology”.

 

Abstract:

Prolactin-producing tumors represent nearly half of all pituitary tumors. The noticeable rate of aggressive clinical behavior in males with macroprolactinoma necessitates identifying novel genes and proteins which play a role in the process of tumorigenesis, tumor invasion to adjacent structures and resistance to medical treatment. ERα36 expression which is a novel splice variant of traditional ERα66 receptor has not been evaluated in the pituitary gland which is highly responsive to estrogen. In this cohort study, tumor samples from 62 patients with prolactinoma who underwent surgery during a period of eight years were evaluated for immunohistochemistry. ERα36, ERα66, Ki67 and p53 were measured by semi-quantitative immunoreactive score. A wide expression of ERα36 even more than ERα66 was found in normal pituitaries.  This may imply the importance of non-genomic signaling pathway of estrogen in the pituitary. The scoring results of Ki67 showed that tumor proliferation rate was higher in males. Males also showed a greater mitotic count than women. Males presented larger and invasive tumors. There were no significant sex-related differences in the expression of the estrogen receptors and p53. Taken together, the results indicate that Macroprolactimomas in males are more aggressive than females. However, there were no significant difference in ERα36 and ERα66 expression between males’and females’ tumors.

Break: Lunch Break 12:20-13:40
Speaker
Biography:

Maha M. Deif, currently working as a professor in department of Faculty of medicine at Alexandria University in Egypt.

Abstract:

Novel evidence showed that the high fructose consumption impaired cognitive abilities and disrupted the insulin signaling. High-fat diet consumption also caused learning impairment. Learning and memory deficit were induced by β-amyloid peptide 1-42 was documented in recent studies. Based on this assumption, the aim of the present study was to test the hypothesis that diet would modulate β-amyloid 1-42 deposition in the brain, which may be implicated in causing memory deficit. The study was conducted on 30 adult male albino rats, aged 12-14 months, ranging in body weight from 150–200 g, divided into 3 groups (n=10), each was given one of 3 different diets: group I given Control diet (CD) consisted of standard chow pellets, group II given high unsaturated-fat diet (HUFD) and group III given high carbohydrate diet (HCD), for the entire test period which lasted for 8 weeks. On the last day of the eight weeks, memory training through water maze test was done. 24 hours later, memory testing was performed after which rats were allowed to fast for 12 hours before being sacrificed. Blood obtained from the jugular vein was collected and plasma was separated for measuring fasting blood glucose and plasma lipids, hippocampus was homogenized and stored for biochemical determinations of β-amyloid 1-42, and superoxide dismutase activity in all groups.

Speaker
Biography:

Muhammad Sibte Hasan Mahmood received his MBBS degree from Rawalpindi Medical College in Pakistan. He has worked as a physician in Pakistan for various health care providers. Since moving to Canada in 2015, he has focused more attention to research and study trials. Working with renowned researchers in various medical fields either under direct or indirect supervisions has offered invaluable experience and learning. His main areas of focus has been drug mechanics and therapeutic modelling. He strives to achieve a long lasting impact in the field of clinical and pharmacologic research and development.

Abstract:

The use of pesticides and insecticides has increased in agricultural field and household etc for pest control, pest management and to prevent diseases caused by insects respectively over a period. Insecticides are also a category of pesticides. Some of the most abundantly used pesticides contain organophosphate compounds as basic ingredient. Organophosphate compounds are ester, amide and thiol derivatives of phosphoric acid. Such compounds are highly toxic and their accumulation in the human body can cause neuro-poisoning. They deactivate the human acetylcholinesterase (AChE) and thus stop the acetylcholine neurotransmission. Although the process is not permanent, it depends upon how much time the interaction between organophosphate compound and AChE has taken before the aging and denaturation of the enzyme starts. Before aging of the enzyme, a group of compounds known as Oximes belonging to the family of amines can be used to reactivate the human acetylcholinesterase.

Oximes are divided into four sub-categories namely: aldoximes, ketoximes, oxime esters and steroid oximes depending upon their chemical orientation. The first oxime was developed by Czech Republic in 1956. Among them, obidoxime and pralidoxime are clinically used for years and are synthesised commercially. Oximes can reactivate the human AChE by removing the phosphate attached to its residues in the catalytic active sides, phosphorylated by organophosphate compounds. In this study, the structures of oximes were obtained from previously performed experiments. The structures were then converted to 2D structures (SDF) via PubChem. The SDF files were then converted to PDB (3D) format using PyRx tool which produced a tertiary structure of the oximes which was a requirement to perform docking. As for the human AChE, the structures of inhibited AChE were downloaded from Protein Data Bank in the PDB format and cleaned using Chimera tool. After preparing the 3D structures, oximes with highest chances of reactivating the inhibited AChE were selected by observing the AChE and oxime interactions. A total of 67 oximes from different categories were selected forming more than 600 conformations of enzyme-ligand complexes. To further improve the properties, characteristics if the toxicity and metabolism of these oximes were also checked using ligplot+ and Vega ZZ.

Our results suggest that, brasofensine, caproxamine, CPCCOEt, Demexiptiline, FERb-033, Milameline, NS-2710, Noxiptiline, Perillartine, Pralidoxime and Salicylaldoxime showed very strong interaction with the receptor and thus were able to reactivate the inhibited AChE.

Speaker
Biography:

Published many papers in Cardiosource, American College of Cardiology Foundation, Case Reports in Clinical Medicine (SCIRP) and Journal of Saudi Heart Association. Special research on Rheumatic fever and Endomyocardial fibrosis in tropical belts, Myxomas, Infective endocarditis, apical hypertrophic cardiomyopathy, Ebstein’s anomaly, Rheumatic Taussig-Bing Heart, Costello syndrome and Tetralogy of Fallot.

Abstract:

Brain abscess is an intraparenchymal infection of brain parenchyma and begins with a localized area of inflammatory change referred to as ‘cerebritis’, progress to immature capsule stage and then to abscess, containing pus encapsulated by a vascularized membrane. The capsule serves to prevent the infective process from becoming generalized and it also create within it an inflammatory “soup” that may impede resolution of the infection. The incidence of brain abscess is about 8% of intracranial masses in developing countries and in cyanotic heart disease, its incidence varies from 5 to 18.7%. In patients with right-to-left shunts, absence of pulmonary phagocytic clearance of pathogens can occur and the ischemic injury from hypoxaemia and polycyathaemia, produce low perfusion areas in the brain which may act as a nidus for infection and anaerobic streptococci are the most common agents isolated in cyanotic heart disease with brain abscess. All abscesses > 1 cm produce positive scans and CT brain appears to be adequate in most cases of brain abscess. Third generation cephalosporins (cefotaxime or ceftriaxone) combined with metronidazole for 2 weeks followed by 4 weeks of oral therapy is the medical treatment of choice for cyanotic brain abscess. Surgical techniques such as drainage via burr-hole, complete excision after craniotomy, migration technique and neuroendoscopic technique with freehand stereotaxy  have also been practiced in the treatment of brain abscess.

Speaker
Biography:

I have receved my pharm D degree in 2011. I am a Pharmacology PhD student at Shahid Beheshti University of Medical Sciences. At the moment i am working on my PhD thesis which explores therapeutic effects of Astaxanthin in spinal cord injury (SCI). I have one paper.

Abstract:

Spinal cord injury (SCI) can lead to temporary or permanent loss of neurologic function.  Nevertheless, the ideal treatment has not found for SCI. Since the SCI is a complex, multifaceted disease process so, combinatorial treatments can be a promising approach. Epidermal neural crest stem cells (EPI-NCSCs) are unique candidates witch isolated from bulge hair follicles in adults due to the possibility of autologous transplantation. We evaluated whether combination of a potent antioxidant such as Astaxanthin (AST) and (EPI-NCSCs) transplantation could affect (SCI). The sever SCI induced by dropping a metal rod onto the exposed dorsal surface of the spinal cord on male rats witch treated by Ast (0.2mM) and EPI-NCSCs (106/10μl PBS) alone and combined. The Basso, Beattie and Bresnahan (BBB) test on days 1, 3, 7, 14, 21, 28, 35 and 42 post-injury was used for assessing of Motor function. The Motor neurons number and the myelin level were investigated on days 14 and 42 using Nissl and Luxol Fast Blue staining. All treatments improved motor function on days 7, 14, 21, 28, 35 and 42 compared to SCI. However combination therapy was more effective than Ast or EPI-NCSCs individually in behavioral improvement. Decreased the motor neurons number following SCI, increased by Ast, Cell and Ast+Cell, but combination therapy significantly had better effects. Although all treatment increased white matter compared to SCI, treatment with Ast+Cell had increased myelin levels.

Vahideh Nasr

Shahid Beheshti University of Medical Sciences, Iran

Title: Allogenic Mesenchymal Stem Cell Therapy for CADASIL Patient: First Clinical Case Report

Time : 16:20-17:00

Speaker
Biography:

Professor Madana Mohiuddin Bonab, pioneer of stem cell Therapy application in the treatment of MS, is one of the authors of this study. She is the best technologist awarded in 13th, Anniversary meeting of Pardis Technology Park in 2015 and Co-author of “Multiple Sclerosis A Mechanistic view“ , “Neuroinflammatiom“  and  “The neurobiology of multiple sclerosis“ (Elsevier).

Abstract:

CADASIL, Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy, is an inherited small vessels disease that characterized by central nervous system dysfunctions caused by mutations in the Notch-3 gene. Clinical manifestations accrue due to brain’s vasculopathy, neurodegeneration, and immune system reaction. We describe here an effective method for treatment of CADASIL by using mesenchymal stem cell therapy. A CADASIL case, 36 years old man, neuroimaging and genetic analysis for Notch-3 confirmed the diagnosis, is reported. In the present case, two stem cell injections have been performed at intervals of three weeks. The patient had no significant complications in the post-transplant period. No immediate or delayed side effects following MSC infusion were observed. He developed neither malignancy nor unwanted cells or any infectious complications 18 months after the transplantation, we performed a Cerebral MRI showed stable cerebral lesions and his gate and balance improved. Anti-HLA Antibody measurement confirmed that the patient's immune system was not stimulated by injected cells.With regard to his neurological symptoms, Scale for the assessment and rating of ataxia (SARA), The Multiple Sclerosis Functional Composite measure (MSFC), Quality of Life Assessment (QOL),   and Cognitive Functioning Status (ACE-R), the patient did not has further deterioration  of his previous clinical status in the follow up period of 18 months. Further studies need to be performed to show the generalizability of the results.