Dysregulation of Rab5-mediated endocytic pathways in Alzheimer's disease

被引：53

作者：

Xu, Wei ^{[1
,2
,3
]}

Fang, Fang ^{[1
,2
,3
]}

Ding, Jianqing ^{[1
,2
]}

Wu, Chengbiao ^{[3
]}

机构：

[1] Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Inst Neurol, Shanghai, Peoples R China

[2] Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Dept Neurol, Shanghai, Peoples R China

[3] Univ Calif San Diego, Dept Neurosci, Med Teaching Facil Rm312,9500 Gilman Dr 0624, San Diego, CA 92103 USA

来源：

TRAFFIC | 2018年 / 19卷 / 04期

基金：

中国国家自然科学基金;

关键词：

Alzheimer's disease; atrophy; axonal dysfunction; axonal transport; endocytosis; neurodegeneration; Rab5; AMYLOID PRECURSOR PROTEIN; CHOLINERGIC BASAL FOREBRAIN; MILD COGNITIVE IMPAIRMENT; GENOME-WIDE ASSOCIATION; PHOSPHATE-BINDING LOOP; RAB5 EFFECTOR EEA1; SMALL GTPASE RAB5; ALPHA-SYNUCLEIN; MOUSE MODEL; A-BETA;

D O I：

10.1111/tra.12547

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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.

引用

页码：253 / 262

页数：10

共 142 条

[1] Nerve growth factor: from the early discoveries to the potential clinical use [J].

Aloe, Luigi ;

Rocco, Maria Luisa ;

Bianchi, Patrizia ;

Manni, Luigi .

JOURNAL OF TRANSLATIONAL MEDICINE, 2012, 10

[2] Distribution and Expression of Picalm in Alzheimer Disease [J].

Baig, Shabnam ;

Joseph, Sally A. ;

Tayler, Hannah ;

Abraham, Richard ;

Owen, Michael J. ;

Williams, Julie ;

Kehoe, Patrick G. ;

Love, Seth .

JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 2010, 69 (10) :1071-1077

[3]

BARBIERI MA, 1994, J BIOL CHEM, V269, P18720

[4]

Beattie EC, 1996, COLD SPRING HARB SYM, V61, P389

[5] Impairments in learning and memory accompanied by neurodegeneration in mice transgenic for the carboxyl-terminus of the amyloid precursor protein [J].

Berger-Sweeney, J ;

McPhie, DL ;

Arters, JA ;

Greenan, J ;

Oster-Granite, ML ;

Neve, RL .

MOLECULAR BRAIN RESEARCH, 1999, 66 (1-2) :150-162

[6] γ-Secretase Inhibition Reduces Spine Density In Vivo via an Amyloid Precursor Protein-Dependent Pathway [J].

Bittner, Tobias ;

Fuhrmann, Martin ;

Burgold, Steffen ;

Jung, Christian K. E. ;

Volbracht, Christiane ;

Steiner, Harald ;

Mitteregger, Gerda ;

Kretzschmar, Hans A. ;

Haass, Christian ;

Herms, Jochen .

JOURNAL OF NEUROSCIENCE, 2009, 29 (33) :10405-10409

[7] Extensive axonal Lewy neurites in Parkinson's disease:: a novel pathological feature revealed by α-synuclein immunocytochemistry [J].

Braak, H ;

Sandmann-Keil, D ;

Gai, WP ;

Braak, E .

NEUROSCIENCE LETTERS, 1999, 265 (01) :67-69

[8] THE SMALL GTPASE RAB5 FUNCTIONS AS A REGULATORY FACTOR IN THE EARLY ENDOCYTIC PATHWAY [J].

BUCCI, C ;

PARTON, RG ;

MATHER, IH ;

STUNNENBERG, H ;

SIMONS, K ;

HOFLACK, B ;

ZERIAL, M .

CELL, 1992, 70 (05) :715-728

[9] Loss of Bin1 Promotes the Propagation of Tau Pathology [J].

Calafate, Sara ;

Flavin, William ;

Verstreken, Patrik ;

Moechars, Diederik .

CELL REPORTS, 2016, 17 (04) :931-940

[10] Alzheimer-like neurodegeneration in aged antinerve growth factor transgenic mice [J].

Capsoni, S ;

Ugolini, G ;

Comparini, A ;

Ruberti, F ;

Berardi, N ;

Cattaneo, A .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (12) :6826-6831

← 1 2 3 4 5 6 7 8 9 10 →