Does Nitric Oxide Synthase Contribute to the Pathogenesis of Alzheimer's Disease? Effects of β-Amyloid Deposition on NOS in Transgenic Mouse Brain with AD Pathology

D. K. Lahiri, D. Chen, Y. W. Ge, M. Farlow, G. Kotwal, A. Kanthasamy, D. K. Ingram, N. H. Greig

Research output: Contribution to journalArticle

19 Scopus citations

Abstract

Oxidative stress is a risk factor for Alzheimer's disease (AD) whose major hallmark includes brain depositions of the amyloid beta peptide (Aβ) derived from the β-amyloid precursor protein (APP). Our aim was to determine whether or not excessive Aβ deposition would alter nitric oxide synthase (NOS) activity, and thereby affect NOS-mediated superoxide formation. We compared NOS activity in brain extracts between Tg mice (expressing APP Swedish double mutation plus presenilin [PS-1] and nontransgenic [nTg] mice. Five brain regions, including cerebral cortex, hippocampus, cerebellum, and striatum from both nTg and Tg mice showed a detectable level of neuronal (n) NOS activity. Cerebellar extracts from both nTg and Tg mice displayed the highest level of nNOS activity, which was fourfold higher than cortical extracts. Although there was an increase in nNOS activity in Tg brain extracts, this did not attain statistical significance. A similar result was obtained for inducible NOS levels. Our results suggest that excess levels of Aβ failed to both trigger NOS activity and change NOS levels.

Original languageEnglish (US)
Pages (from-to)639-642
Number of pages4
JournalAnnals of the New York Academy of Sciences
Volume1010
DOIs
StatePublished - Jan 1 2003

Keywords

  • Aging
  • Beta-protein
  • Dementia
  • Free radicals
  • Neurodegeneration
  • Nitric oxide
  • Oxidative stress
  • ROS

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

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