期刊
CNS & NEUROLOGICAL DISORDERS-DRUG TARGETS
卷 13, 期 1, 页码 112-119出版社
BENTHAM SCIENCE PUBL
DOI: 10.2174/18715273113126660130
关键词
Alzheimer disease; ammonia; amyloid-beta; erythrocyte energy metabolism; oxidative stress
资金
- Russian Ministry of Education and Sciences, Moscow, Russia [4.1311.2011]
- GALLY International Biomedical Research Consulting LLC., San Antonio, TX, USA
A beta 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-beta 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-beta, systemic ammonia, erythrocyte energy metabolism and the role of 2,3-diphosphoglycerate in AD pathogenesis.
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