期刊
JOURNAL OF MOLECULAR NEUROSCIENCE
卷 23, 期 3, 页码 247-254出版社
HUMANA PRESS INC
DOI: 10.1385/JMN:23:3:247
关键词
Alzheimer's disease; apolipoprotein E; clusterin; amyloid
资金
- NIA NIH HHS [AG13956, AG11355, P50-AG05681] Funding Source: Medline
- NINDS NIH HHS [NS034467] Funding Source: Medline
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS034467, R37NS034467] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R37AG013956, R01AG013956, P01AG011355, P50AG005681] Funding Source: NIH RePORTER
The epsilon4 allele of apolipoprotein E APOE is a risk factor for Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA), and the epsilon2 allele is associated with a decreased risk for AD. There is strong evidence to suggest that a major, if not the main, mechanism underlying the link between apoE and both AD and CAA is related to the ability of apoE to interact with the amyloid-beta (Abeta) peptide and influence its clearance, aggregation, and conformation. In addition to a number of in vitro studies supporting this concept, in vivo studies with amyloid precursor protein (APP) transgenic mice indicate that apoE and a related molecule, clusterin (also called apolipoprotein J), have profound effects on the onset of Abeta deposition, as well as the local toxicity associated with AD deposits both in the brain parenchyma and in cerebral blood vessels. Taken together, these studies suggest that altering the expression of apoE and clusterin in the brain or the interactions between these molecules and Abeta would alter AD pathogenesis and provide new therapeutic avenues for prevention or treatment of CAA and AD.
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