期刊
TRAFFIC
卷 19, 期 4, 页码 253-262出版社
WILEY
DOI: 10.1111/tra.12547
关键词
Alzheimer's disease; atrophy; axonal dysfunction; axonal transport; endocytosis; neurodegeneration; Rab5
类别
资金
- Shanghai Municipal Education Commission [12ZZ115]
- National Natural Science Foundation of China [81600920, 81171200]
- Center for Scientific Review
- Ministry of Science and Technology of the People's Republic of China [2014CB965002, 2012BAI10B03]
- Science and Technology Commission of Shanghai Municipality [13JC1401502, 13140904000]
- Tau Consortium
- Larry L. Hillblom Foundation
- Down Syndrome Research and Treatment Foundation
- NIH UCSD ADRC P50 Pilot grant
- NIH [PN2EY016525]
Increasing evidence has pointed to that dysregulation of the endo-lysosomal system is an early cellular phenotype of pathogenesis for Alzheimer's disease (AD). Rab5, a small GTPase, plays a critical role in mediating these processes. Abnormal overactivation of Rab5 has been observed in post-mortem brain samples of Alzheimer's patients as well as brain samples of mouse models of AD. Recent genome-wide association studies of AD have identified RIN3 (Ras and Rab interactor 3) as a novel risk factor for the disease. RIN3 that functions as a guanine nucleotide exchange factor for Rab5 may serve as an important activator for Rab5 in AD pathogenesis. In this review, we present recent research highlights on the possible roles of dysregulation of Rab5-mediated endocytic pathways in contributing to early pathogenesis of AD.
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