DNA base excision repair activities in mouse models of Alzheimer's disease

Lior Weissman, Nadja C. de Souza-Pinto, Mark P. Mattson, Vilhelm A. Bohr

Research output: Contribution to journalArticlepeer-review

Abstract

Alzheimer's disease (AD) has been correlated with elevated levels of oxidative DNA damage. Base excision repair (BER) is the main repair pathway for the removal of oxidative DNA base modifications. We have recently found significant functional deficiencies in BER in brains of sporadic AD and amnestic mild cognitive impairment patients. In this study we tested whether altered BER activities are associated with appearance of symptoms in different brain regions of pre-symptomatic and symptomatic mice harboring mutant APP alone or in combination with Tau and PS1. Our results suggest that unlike in humans, the development of AD-like pathology in the studied mouse models is not associated with deficiencies in BER.

Original languageEnglish (US)
Pages (from-to)2080-2081
Number of pages2
JournalNeurobiology of Aging
Volume30
Issue number12
DOIs
StatePublished - Dec 2009
Externally publishedYes

Keywords

  • Alzheimer's disease
  • DNA repair
  • Oxidative DNA damage
  • Oxidative stress

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)
  • Aging
  • Developmental Biology
  • Geriatrics and Gerontology

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