The aid of ephedrine HCL, curcumin and turmerone in neurogenesis and inhibition of beta-amyloid plaques in transgenic mouse models

Abstract

Event Abstract Back to Event The aid of ephedrine HCL, curcumin and turmerone in neurogenesis and inhibition of beta-amyloid plaques in transgenic mouse models Keerthi Paramasivam1* 1 Harvard University, Department of Neurosciences, Harvard Medical School, United States This study was done to demonstrate the effects of ephedrine HCL, turmerone and curcumin in neurogenesis and inhibition of beta amyloids in transgenic mice. The transgenic mouse models used contain mutations associated with familial Alzheimer's disease (APP Swedish, MAPT P301L, and PSEN1 M146V). These mice develop age-related, progressive neuropathology including plaques and tangles. Ten-month-old male and female APPSw Tg+ and Tg- mice from 12 litters were randomly split between treatment groups. Tg+ mice were fed either with chow containing a low dose of curcumin (160 ppm;n=9), a high dose of curcumin (5000ppm;n=6) or no drug (n=8) for 6 months. Mice with low and high dose of curcumin were given specific doses of 0.02% ephedrine HCL injection every 72 hours and underwent a single intracerebroventricular injection of 3mg turmerone. To evaluate whether curcumin treatment affected plaque pathology, cryostat hemibrain sections from Tg+ control and Tg+ low-dose curcumin-treated mice were immunostained with an antibody against Aß1–13 (DAE). Two-factor ANOVA revealed a significant reduction in plaque burden in curcumin, ephedrine HCL and turmerone treated animals [F (1,60) = 4.74; p=0.03], in which amyloid burden was decreased by 43.6% in treated animals compared with untreated animals. Soluble Aß in Tg+ untreated and Tg+ low-dose curcumin mice were measured by sandwich ELISA. Two-way ANOVA showed significant treatment effects in decreasing the levels of soluble Aß (*p < 0.05). Underlying mechanistic pathways that might link curcumin treatment to increased cognition and neurogenesis via exon array analysis of cortical and hippocampal mRNA transcription showed a positive result. Keywords: Cognition, Neurogenesis, neurodegeneration, in vivo, beta amyloid Conference: 14th Meeting of the Asian-Pacific Society for Neurochemistry, Kuala Lumpur, Malaysia, 27 Aug - 30 Aug, 2016. Presentation Type: Free Paper Session 1: Novel Therapy for Brain Disorders Topic: 14th Meeting of the Asian-Pacific Society for Neurochemistry Citation: Paramasivam K (2016). The aid of ephedrine HCL, curcumin and turmerone in neurogenesis and inhibition of beta-amyloid plaques in transgenic mouse models. Conference Abstract: 14th Meeting of the Asian-Pacific Society for Neurochemistry. doi: 10.3389/conf.fncel.2016.36.00099 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 04 Aug 2016; Published Online: 11 Aug 2016. * Correspondence: Dr. Keerthi Paramasivam, Harvard University, Department of Neurosciences, Harvard Medical School, Boston, MA, United States, keerthiparamasivam2938@gmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Keerthi Paramasivam Google Keerthi Paramasivam Google Scholar Keerthi Paramasivam PubMed Keerthi Paramasivam Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.