TOR on the brain

被引:110
作者
Garelick, Michael G. [1 ]
Kennedy, Brian K. [1 ,2 ,3 ]
机构
[1] Univ Washington, Dept Biochem, Seattle, WA 98195 USA
[2] Buck Inst Age Res, Novato, CA 94945 USA
[3] Guangdong Med Coll, Aging Res Inst, Dongguan 523808, Guangdong, Peoples R China
关键词
Rapamycin; TOR; Neurodegeneration; Alzheimer's disease; Huntington's disease; Parkinson's disease; LONG-TERM POTENTIATION; PHOSPHOINOSITIDE 3-KINASE-AKT-MAMMALIAN TARGET; ELONGATION-FACTOR; 1A; P70; S6; KINASE; MAMMALIAN TARGET; SYNAPTIC PLASTICITY; ALZHEIMERS-DISEASE; SIGNALING PATHWAY; PROTEIN-SYNTHESIS; LIFE-SPAN;
D O I
10.1016/j.exger.2010.08.030
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
Signaling by target of rapamycin (mTOR in mammals) has been shown to modulate lifespan in several model organisms ranging from yeast to mice. In mice, reduced mTOR signaling by chronic rapamycin treatment leads to life span extension, raising the possibility that rapamycin and its analogs may benefit the aging brain and serve as effective treatments of age-related neurodegenerative diseases. Here, we review mTOR signaling and how neurons utilize mTOR to regulate brain function, including regulation of feeding, synaptic plasticity and memory formation. Additionally, we discuss recent findings that evaluate the mechanisms by which reduced mTOR activity might benefit the aging brain in normal and pathological states. We will focus on recent studies investigating mTOR and Alzheimer's disease, Parkinson's disease, and polyglutamine expansion syndromes such as Huntington's disease. (C) 2010 Elsevier Inc. All rights reserved.
引用
收藏
页码:155 / 163
页数:9
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