期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 19, 期 1, 页码 341-353出版社
IOS PRESS
DOI: 10.3233/JAD-2010-1222
关键词
Alzheimer's disease; amyloid; early Alzheimer's disease; mild cognitive impairment; oxidative stress; proteomics
资金
- National Institute of Health [AG05119, AG10836, AG029839]
- NATIONAL INSTITUTE ON AGING [R01AG029839, P01AG010836] Funding Source: NIH RePORTER
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is characterized pathologically by the presence of senile plaques, neurofibrillary tangles, and synapse loss. Increasing evidence supports a role of amyloid beta-peptide (A beta)-induced oxidative stress in the progression and pathogenesis of AD. In this review, we summarize evidence for a role of oxidative stress in the progression of AD by comparing the appearance of the same oxidized brain proteins from subjects with mild cognitive impairment (MCI), early AD (EAD), and late-stage AD, and relating these findings to the reported AD pathology. The identification of oxidized brain proteins in common in MCI, EAD, and AD brain suggest that certain key pathways are triggered and may be involved in the progression of AD. Exploring these pathways in detail may provide clues for better understanding the pathogenesis and progression of AD and also for the development of effective therapies to treat or delay this dementing disorder.
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