Journal
JOURNAL OF NEUROCHEMISTRY
Volume 89, Issue 5, Pages 1308-1312Publisher
WILEY
DOI: 10.1111/j.1471-4159.2004.02455.x
Keywords
Alzheimer's disease; beta-amyloid; manganese superoxide dismutase; oxidative stress; transgenic mice
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Funding
- NIA NIH HHS [AG 00798, AG 20729, AG 14930] Funding Source: Medline
- NINDS NIH HHS [NS 045677, NS 02037] Funding Source: Medline
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A growing body of evidence suggests a relationship between oxidative stress and beta-amyloid (Abeta) peptide accumulation, a hallmark in the pathogenesis of Alzheimer's disease (AD). However, a direct causal relationship between oxidative stress and Abeta pathology has not been established in vivo. Therefore, we crossed mice with a knockout of one allele of manganese superoxide dismutase (MnSOD), a critical antioxidant enzyme, with Tg19959 mice, which overexpress a doubly mutated human beta-amyloid precursor protein (APP). Partial deficiency of MnSOD, which is well established to cause elevated oxidative stress, significantly increased brain Abeta levels and Abeta plaque burden in Tg19959 mice. These results indicate that oxidative stress can promote the pathogenesis of AD and further support the feasibility of antioxidant approaches for AD therapy.
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