Amyloid-β deposition in Alzheimer transgenic mice is associated with oxidative stress

Mark A. Smith, Keisuke Hirai, Karen Hsiao, Miguel A. Pappolla, Peggy L.R. Harris, Sandra L. Siedlak, Massimo Tabaton, George Perry

Research output: Contribution to journalArticlepeer-review

502 Scopus citations


Increased awareness for a role of oxidative stress in the pathogenesis of Alzheimer's disease has highlighted the issue of whether oxidative damage is a fundamental step in the pathogenesis or instead results from disease- associated pathology. In vitro experiments support both possibilities: Oxidative stress increases amyloid-β production, and, conversely, amyloid- β increases oxidative damage. To address the relationship between amyloid- β and oxidative stress in vivo, we examined, using an array of oxidative markers, transgenic mice that overexpress amyloid-β precursor protein and, as in Alzheimer's disease, develop characteristic amyloid-β deposits within the brain parenchyma. Transgenic animals show the same type of oxidative damage that is found in Alzheimer's disease, and it is important that this damage directly correlates with the presence of amyloid-β deposits. The significance of these studies is twofold. First, they provide evidence that amyloid-β and oxidative damage are inextricably linked in vivo. Second, they support the use of transgenic animals for the development of antioxidant therapeutic strategies.

Original languageEnglish (US)
Pages (from-to)2212-2215
Number of pages4
JournalJournal of neurochemistry
Issue number5
StatePublished - May 1998
Externally publishedYes


  • Alzhelmer's disease
  • Oxidative stress
  • Transgenic mouse

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience


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