Reactive oxygen species mediate cellular damage in Alzheimer disease

G. Perry*, R. J. Castellani, K. Hirai, M. A. Smith

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

174 Scopus citations

Abstract

The two most striking features of Alzheimer disease are (i) the multitude of abnormalities affecting essentially every system and (ii) the strict age dependence. Recent work suggests that both features are linked to increased oxidative stress that damages lipids, proteins and nucleic acids and results in redox-active metal accumulations, mitochondrial damage and formation of advanced glycation endproducts. Interestingly, β-protein precursor, amyloid-β, presenilins, and apolipoprotein E have all been linked to reactive oxygen species production or apoptosis, a process intimately associated with oxidative stress. In therapeutics, the commonality between a number of efficacious agents appears to be oxidative stress reduction. Therefore, we contend that oxidative stress is the element that links the multitude of changes in Alzheimer disease and that a reduction of oxidative stress will have a dramatic effect on reducing the incidence or progression of Alzheimer disease.

Original languageEnglish (US)
Pages (from-to)45-55
Number of pages11
JournalJournal of Alzheimer's Disease
Volume1
Issue number1
DOIs
StatePublished - 1998
Externally publishedYes

ASJC Scopus subject areas

  • Neuroscience(all)
  • Clinical Psychology
  • Geriatrics and Gerontology
  • Psychiatry and Mental health

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