Journal of Neuroscience and Neurological Disorders Open Access HTTPS://WWW.HEIGHPUBS.ORG ISSN 2639-3220 ABSTRACT Stroke and neurodegenerative diseases including Alzheimer’s disease (AD) are responsible for a major proportion of mortalities in the elderly. We have previously investigated novel mechanism-based therapies of AEURA in cell culture models against viral infection and in glutamate excitotoxity. In our new studies, we propose that the homeopathic formula AEURA could serve as a potential therapeutic agent for stroke & for AD. In examining AEURA treatment of PC12 cells exposed to glutamate excitotoxicity, hypoxia /re-oxygenation injury and A-Beta toxicity. We demonstrated an increased survival rate in AEURA treated cells by comparison to control cells. In examining the therapeutic potential of AEURA in PC12 cells this homeopathic agent was found to be neuroprotective against either glutamate induced toxicity, hypoxia /re-oxygenation stress or cell stress resulting from viral infection (with either HSV-1 or rhinovirus). Our ongoing studies involve examining the neuroprotective potential AEURA in vivo using rodent models of stroke & AD. Research Article Protective functions of AEURA in Cell Based Model of Stroke and Alzheimer disease Jigar Modi 1,3 Ahmed Altamimi 1 , Ashleigh Morrell 1 , Hongyuan Chou 1 , Janet Menzie 1 , Andrew Weiss 4 , Michael L Marshall 4 , Andrew Li 1 , Howard Prentice 1-3 * and Jang-Yen Wu 1-3 * ¹Department of Biomedical Sciences, Charles E. Schmidt College of Medicine, Florida Atlantic University, Boca Raton, FL 33431, USA ²Program in Integrative Biology, Florida Atlantic University, Boca Raton, FL 33431, USA ³Center of Complex Systems and Brain Sciences, Florida Atlantic University, Boca Raton, FL 33431, USA ⁴AEURA Trust, 2525 Arapahoe Ave E4-138, Boulder, Colorado 80302, USA *Address for Correspondence: Howard Prentice, PhD, Department of Biomedical Sciences, Charles E. Schmidt College of Medicine, Florida Atlantic University, Boca Raton, FL 33431, Tel: 561-297-0362; Fax: 561-297-2221; Email: hprentic@fau.edu Jang-Yen Wu, PhD, Department of Biomedical Sciences, Charles E. Schmidt College of Medicine, Florida Atlantic University, Boca Raton, FL 33431, Tel: 561-297-0167; Fax: 561-297-2221; Email: jwu@fau.edu Submitted: 04 May 2017 Approved: 05 June 2017 Published: 06 June 2017 Copyright: 2017 Modi J, et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Keywords: Alzheimer’s disease; Stroke; AEURA; Glutamate; Hypoxia; Amyloid Beta (A-Beta) How to cite this article: Modi J, Altamimi A , Morrell A, Chou H, Menzie J, et al. Protective functions of AEURA in Cell Based Model of Stroke and Alzheimer disease. J Neurosci Neurol Disord. 2017; 1: 016- 023. https://doi.org/10.29328/journal.jnnd.1001003 INTRODUCTION Stroke A stroke occurs when blood supply is blocked to part of the brain or when a blood vessel in the brain ruptures. In both cases, parts of the brain become damaged or die. A stroke can cause permanent brain damage, long-term disability, or even mortality [1]. Stroke is the 5th leading cause of death in the US, with one person dying every 4 minutes. For African Americans, stroke is the 3rd leading cause of death (Xu et al., 2007). Stroke is also a leading cause of serious long-term incapacity. Stroke decrease mobility in more than half of stroke survivors age 65 and over. Roughly 800,000 people have a stroke each year; almost one every 40 seconds. About 87% of all strokes are ischemic strokes, in which blood ϐlow to the brain is restricted or blocked [2]. An experimental study has revealed that more than 60% of patients develop hypoxia within the ϐirst 60 hours after stroke [3]. Stroke or ischemia leads to an increase in the extracellular concentrations of excitatory amino acids, mainly in glutamate [4,5]. This increase in glutamate could be allied to increasing release from neurons, resulting from energy failure, or to reducing clearance of glutamate by glial transporters. An increased production of free radicals and other reactive species in stroke leads to oxidative stress