Mitochondrial trafficking in neuropsychiatric diseases

被引：16

作者：

Deheshi, Samineh ^{[1
]}

Pasqualotto, Bryce A. ^{[1
]}

Rintoul, Gordon L. ^{[1
]}

机构：

[1] Simon Fraser Univ, Dept Biol Sci, Burnaby, BC V5A 1S6, Canada

来源：

NEUROBIOLOGY OF DISEASE | 2013年 / 51卷

基金：

加拿大自然科学与工程研究理事会;

关键词：

Mitochondria; Neuropsychiatric disorders; Alzheimer's disease; Schizophrenia; Depression; Mitochondrial trafficking; Mitochondrial transport; CHILDHOOD-ONSET SCHIZOPHRENIA; IMPAIRED AXONAL-TRANSPORT; ALZHEIMERS-DISEASE; A-BETA; PROTEIN; DISC1; TAU; MOVEMENT; CALCIUM; DYSFUNCTION;

D O I：

10.1016/j.nbd.2012.06.015

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Mitochondria have numerous roles in healthy neuronal functioning and in neuronal injury mechanisms. They are quite dynamic organelles in that they fuse, divide and move throughout axons and dendrites. The mechanisms of mitochondrial motility have received much attention, however the significance of the dynamic nature of mitochondria in neurons is unclear. Nonetheless, deficits in mitochondrial trafficking have been implicated in numerous neurodegenerative disorders. The role of aberrant mitochondrial trafficking in neuropsychiatric disorders is not as well understood, but may involve similar mechanisms. In this review we examine the evidence which implicates changes in mitochondrial trafficking in the pathogenesis of neuropsychiatric disorders and hypothesize how defective mitochondrial transport may contribute to disease mechanisms. (C) 2012 Elsevier Inc. All rights reserved.

引用

页码：66 / 71

页数：6

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