Evidence of oxidative damage in Alzheimer’s disease brain: central role for amyloid β-peptide

Dept of Chemistry, Center of Membrane Sciences and Sanders-Brown Center on Aging, University of Kentucky, Lexington 40506-0055, USA.
Trends in Molecular Medicine (Impact Factor: 10.11). 01/2002; 7(12):548-54. DOI: 10.1016/S1471-4914(01)02173-6
Source: PubMed

ABSTRACT Amyloid beta-peptide (Abeta) is heavily deposited in the brains of Alzheimer's disease (AD) patients. Free-radical oxidative stress, particularly of neuronal lipids, proteins and DNA, is extensive in those AD brain areas in which Abeta is abundant. Recent research suggests that these observations might be linked, and it is postulated that Abeta-induced oxidative stress leads to neurodegeneration in AD brain. Consonant with this postulate, Abeta leads to neuronal lipid peroxidation, protein oxidation and DNA oxidation by means that are inhibited by free-radical antioxidants. Here, we summarize current research on phospholipid peroxidation, as well as protein and DNA oxidation, in AD brain, and discuss the potential role of Abeta in this oxidative stress.

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Available from: Alessandra Castegna, May 26, 2015
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