期刊
NATURE REVIEWS NEUROSCIENCE
卷 10, 期 5, 页码 333-344出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nrn2620
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资金
- NIA NIH HHS [R01 AG031784, R01 AG027924-03, R01 AG031784-01, P01 AG030128-01A28719, R01 AG027924-03S1, R01 AG027924-04, P01 AG030128-01A28715, R01AG027924, R01 AG027924-01, P01 AG030128, R01AG031784, R01 AG031784-02, R01 AG027924-02, R01 AG027924-05, R01 AG027924] Funding Source: Medline
- NATIONAL INSTITUTE ON AGING [R01AG031784, R01AG027924, P01AG030128] Funding Source: NIH RePORTER
The vast majority of Alzheimer's disease (AD) cases are late-onset and their development is probably influenced by both genetic and environmental risk factors. A strong genetic risk factor for late-onset AD is the presence of the epsilon 4 allele of the apolipoprotein E (APOE) gene, which encodes a protein with crucial roles in cholesterol metabolism. There is mounting evidence that APOE4 contributes to AD pathogenesis by modulating the metabolism and aggregation of amyloid-beta peptide and by directly regulating brain lipid metabolism and synaptic functions through APOE receptors. Emerging knowledge of the contribution of APOE to the pathophysiology of AD presents new opportunities for AD therapy.
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