Oxidative processes in Alzheimer's disease: the role of abeta-metal interactions

Exp Gerontol. 2000 Jul;35(4):445-51. doi: 10.1016/s0531-5565(00)00112-1.

Abstract

Alzheimer's disease is characterized by signs of a major oxidative stress in the neocortex and the concomitant deposition of Amyloid beta (Abeta). Abeta is a metalloprotein that binds copper, and is electrochemically active. Abeta converts molecular oxygen into hydrogen peroxide by reducing copper or iron, and this may lead to Fenton chemistry. Hydrogen peroxide is a freely permeable prooxidant that may be responsible for many of the oxidative adducts that form in the Alzheimer-affected brain. The electrochemical activity of various Abeta species correlates with the peptides' neurotoxicity in cell culture, and participation in the neuropathology of Alzheimer's disease. These reactions present a novel target for Alzheimer therapeutics.

Publication types

  • Review

MeSH terms

  • Alzheimer Disease / metabolism*
  • Amyloid beta-Peptides / physiology
  • Antioxidants / metabolism
  • Humans
  • Metals / metabolism
  • Neurotoxins / metabolism
  • Oxidation-Reduction
  • Reactive Oxygen Species / metabolism

Substances

  • Amyloid beta-Peptides
  • Antioxidants
  • Metals
  • Neurotoxins
  • Reactive Oxygen Species