Abstract

Abstract A growing body of evidence suggests a relationship between oxidative stress and β‐amyloid (Aβ) peptide accumulation, a hallmark in the pathogenesis of Alzheimer's disease (AD). However, a direct causal relationship between oxidative stress and Aβ 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 β‐amyloid precursor protein (APP). Partial deficiency of MnSOD, which is well established to cause elevated oxidative stress, significantly increased brain Aβ levels and Aβ 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.

Keywords

Oxidative stressPathogenesisKnockout mouseSuperoxide dismutaseAmyloid precursor proteinAlzheimer's diseaseAmyloid (mycology)AntioxidantAmyloid betaBiologyEndocrinologyInternal medicineMedicineImmunologyDiseasePathologyBiochemistryGene

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Year
2004
Type
article
Volume
89
Issue
5
Pages
1308-1312
Citations
273
Access
Closed

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Feng Li, Noel Y. Calingasan, Fangmin Yu et al. (2004). Increased plaque burden in brains of APP mutant MnSOD heterozygous knockout mice. Journal of Neurochemistry , 89 (5) , 1308-1312. https://doi.org/10.1111/j.1471-4159.2004.02455.x

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DOI
10.1111/j.1471-4159.2004.02455.x