Day 1 :
GALLY International Biomedical Research Institute Inc, USA
Gjumrakch Aliev, MD, PhD is President of “GALLY” International Biomedical Research Institute Inc., San Antonio, Texas, USA. He also holds appointment with the University of Atlanta, Atlanta, Georgia, USA as a Professor of Cardiovascular, Neuropathology, Gerontology, Health Science and Healthcare Administration, and Leading Researcher in the Institute of Physiologically Active Compounds, Russian Academy of Sciences, Chernogolovka, Moscow Region, Russia. He received his MD in 1982, from the Baku Medical University (former USSR) with cum laude. Then, he accomplished his PhD in Cardiovascular Diseases from the prestigious Russian Academy of the Medical Sciences, Moscow, Russia in 1988 with cum laude. He received Post-doctoral Training with Professor G. Burnstock in the University College of the London. He authored and coauthored more than 500 publications in the fields of neurodegenerative diseases research (Alzheimer disease), as well as cardio- and cerebrovascular disease, cancer and electron microscopy. He is an outstanding teacher, scholar and a renowned scientist in the area of cellular molecular physiology, and cardiovascular and neurodegeneration-mediated pathologies and drug development including Alzheimer disease. He is nationally and internationally reputed in his area.
It has been well documented that post-traumatic stress disorder (PTSD) is an anxiety disorder that develops after experiencing trauma. Unfortunately, actual therapies do not help majority of patients with PTSD. Moreover, extinguished fear memories usually reappear in the individuals when exposed to trauma cues. New drugs to reduce the impact of conditioned cues in eliciting abnormal fear responses are urgently required. Cotinine, the main metabolite of nicotine, decreased anxiety and depressive-like behavior, and enhanced fear extinction in mouse models of PTSD. Cotinine, considered a positive modulator of the α7 nicotinic acetylcholine receptor (α7nAChR), enhances fear extinction in rodents in a manner dependent on the activity of the αnAChRs. Cotinine stimulates signaling pathways downstream of α7nAChR including the protein kinase B (Akt)/glycogen synthase kinase 3β (GSK3β) pathway and the extracellular signal-regulated kinases (ERKs). The stimulation of these factors promotes synaptic plasticity and the extinction of fear. In this lecture, we will discuss the hypothesis that cotinine relieves PTSD symptoms and facilitates fear memory extinction by promoting brain plasticity through the positive modulation of presynaptic nAChRs and its effectors in the brain.
Chief scientific officer
Premier Micronutrient Corporation
Keynote: Simultaneous activation of Nrf2 and elevation of antioxidant compounds for reducing oxidative stress and chronic inflammation in human Alzheimer’s disease
Time : 10:30-11:00
Kedar N Prasad obtained PhD in Radiation Biology from the University of Iowa and a Post-doctoral Training at the Brookhaven National Laboratory. He was Professor at the University of Colorado, published over 250 papers in prestigious peer-reviewed journals and wrote 25 reference books on radiobiology, nutrition in neurodegenerative disease and cancer. In 1982, he was invited by the Nobel Prize Committee to nominate a candidate for the Nobel Prize in Medicine. He is former President of the International Society for Nutrition and Cancer and Chief Scientific Officer of the Premier Micronutrient Corporation. Currently, he is an independent Consultant.
Biochemical and genetic defects that initiate and promote Alzheimer’s disease (AD) include: (a) Increased oxidative stress, (b) chronic inflammation (c) mitochondrial dysfunction, (d) Aß1-42 peptides generated from the amyloid precursor protein (APP), (e) proteasome inhibition, and (f) mutations in APP, presenilin-1 and presenilin-2 genes. Increased oxidative stress precedes other defects. Oxidative damage induces chronic inflammation. Therefore, reducing these defects simultaneously may decrease the development and progression of AD. Studies using individual antioxidants produced consistent benefits in animal models but not in human AD. Individual antioxidant is oxidized in a high oxidative environment of AD, and acts as a pro-oxidant, and it cannot simultaneously elevate antioxidant enzymes and antioxidant compounds. This paper proposes that simultaneous elevation of the levels of antioxidant enzymes and antioxidant compounds may be necessary for optimally reducing oxidative stress and chronic inflammation in human AD. Supplementation enhances antioxidant compounds; but an elevation of the levels of antioxidant enzymes requires activation of Nrf2 (nuclear transcriptional factor-2). During acute oxidative stress, an activation of Nrf2 requires ROS; however, this mechanism impaired during chronic oxidative stress. Antioxidants activate Nrf2 without ROS stimulation. MicroRNAs that are evolutionary conserved small single-stranded RNAs formed from the non-coding region of DNA, regulate activation of Nrf2. The up-regulated microRNAs cause neurodegeneration by multiple mechanisms including decreasing Nrf2 levels. Antioxidant-induced up-regulated microRNAs activates Nrf2 by reducing Keap1 levels. Author has proposed a mixture of micronutrients that would simultaneously and optimally reduce oxidative stress and chronic inflammation by activating Nrf2 and enhancing the levels of antioxidants in AD.