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CNS & Neurological Disorders - Drug Targets


ISSN (Print): 1871-5273
ISSN (Online): 1996-3181

Pathogenesis of Alzheimer Disease: Role of Oxidative Stress, Amyloid-β Peptides, Systemic Ammonia and Erythrocyte Energy Metabolism

Author(s): Elena A. Kosenko, Iliya N. Solomadin, Lyudmila A. Tikhonova, V. Prakash Reddy, Gjumrakch Aliev and Yury G. Kaminsky

Volume 13, Issue 1, 2014

Page: [112 - 119] Pages: 8

DOI: 10.2174/18715273113126660130

Price: $65


Aβ exerts prooxidant or antioxidant effects based on the metal ion concentrations that it sequesters from the cytosol; at low metal ion concentrations, it is an antioxidant, whereas at relatively higher concentration it is a prooxidant. Thus Alzheimer disease (AD) treatment strategies based solely on the amyloid-β clearance should be re-examined in light of the vast accumulating evidence that increased oxidative stress in the human brains is the key causative factor for AD. Accumulating evidence indicates that the reduced brain glucose availability and brain hypoxia, due to the relatively lower concentration of ATP and 2,3-diphosphoglycerate, may be associated with increased concentration of endogenous ammonia, a potential neurotoxin in the AD brains. In this review, we summarize the progress in this area, and present some of our ongoing research activities with regard to brain Amyloid-β, systemic ammonia, erythrocyte energy metabolism and the role of 2,3-diphosphoglycerate in AD pathogenesis.

Keywords: Alzheimer disease, ammonia, amyloid-β, erythrocyte energy metabolism, oxidative stress.

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