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

Trends Mol Med. 2001 Dec;7(12):548-54. doi: 10.1016/s1471-4914(01)02173-6.

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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Alzheimer Disease / genetics
  • Alzheimer Disease / metabolism*
  • Amyloid beta-Peptides / metabolism*
  • Brain / metabolism
  • DNA / metabolism
  • Free Radicals / metabolism*
  • Humans
  • Lipid Peroxidation
  • Nerve Tissue Proteins / chemistry
  • Nerve Tissue Proteins / metabolism
  • Oxidative Stress*
  • RNA / metabolism

Substances

  • Amyloid beta-Peptides
  • Free Radicals
  • Nerve Tissue Proteins
  • RNA
  • DNA