期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 21, 期 5, 页码 -出版社
MDPI
DOI: 10.3390/ijms21051666
关键词
Alzheimer's disease pathogenesis; diagnostic biomarkers for Alzheimer disease; DNA damage response; DNA damage repair
资金
- Cancer Research Society
- Canadian Cancer Society [319412]
- CIHR
- Urological Cancer Center for Research and Innovation (UCCRI)
- Ontario Graduate Scholarships
- Research Institute of St Joe's Hamilton
Alzheimer's disease (AD) is the most common type of neurodegenerative disease. Its typical pathology consists of extracellular amyloid-beta (A beta) plaques and intracellular tau neurofibrillary tangles. Mutations in the APP, PSEN1, and PSEN2 genes increase A beta production and aggregation, and thus cause early onset or familial AD. Even with this strong genetic evidence, recent studies support AD to result from complex etiological alterations. Among them, aging is the strongest risk factor for the vast majority of AD cases: Sporadic late onset AD (LOAD). Accumulation of DNA damage is a well-established aging factor. In this regard, a large amount of evidence reveals DNA damage as a critical pathological cause of AD. Clinically, DNA damage is accumulated in brains of AD patients. Genetically, defects in DNA damage repair resulted from mutations in the BRAC1 and other DNA damage repair genes occur in AD brain and facilitate the pathogenesis. Abnormalities in DNA damage repair can be used as diagnostic biomarkers for AD. In this review, we discuss the association, the causative potential, and the biomarker values of DNA damage in AD pathogenesis.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据