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Dysregulation of Rab5‐mediated endocytic pathways in Alzheimer's disease
Author(s) -
Xu Wei,
Fang Fang,
Ding Jianqing,
Wu Chengbiao
Publication year - 2018
Publication title -
traffic
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.677
H-Index - 130
eISSN - 1600-0854
pISSN - 1398-9219
DOI - 10.1111/tra.12547
Subject(s) - guanine nucleotide exchange factor , endocytic cycle , pathogenesis , biology , rab , gtpase , phenotype , disease , presenilin , neuroscience , small gtpase , activator (genetics) , alzheimer's disease , signal transduction , microbiology and biotechnology , immunology , endocytosis , genetics , gene , cell , medicine , pathology
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.