Brain Aging: Hsp90 and Neurodegenerative Diseases

被引:11
|
作者
Wang, Kun [1 ,2 ,3 ,4 ]
Shang, Yu [1 ,2 ,3 ,4 ]
Dou, Fei [1 ,2 ,3 ,4 ]
机构
[1] Beijing Normal Univ, State Key Lab Cognit Neurosci & Learning, Beijing, Peoples R China
[2] Beijing Normal Univ, Coll Life Sci, IDG McGovern Inst Brain Res, Beijing, Peoples R China
[3] Beijing Normal Univ, Minist Educ, Coll Life Sci, Key Lab Cell Proliferat & Regulat Biol, Beijing, Peoples R China
[4] Beijing Normal Univ, Ctr Collaborat & Innovat Brain & Learning Sci, Beijing, Peoples R China
关键词
Molecular chaperone; Heat shock protein; Proteostasis; Brain aging; HEAT-SHOCK RESPONSE; ALZHEIMERS-DISEASE; STRESS RESPONSES; CHAPERONES; PROTEINS; HEAT-SHOCK-PROTEIN-90; EXPRESSION; ALPHA; PROTEOSTASIS; ACTIVATION;
D O I
10.1007/978-981-13-1117-8_6
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
The brain is the most complex organ in the human body and the main component of the central nervous system. Because it lacks the ability of regeneration, age is a major risk factor for most common neurodegenerative diseases, which caused an irreversible cognitive impairment. It has been shown that the function of molecular chaperones, majorly heat shock proteins, was compromised and then causes the imbalance of protein homeostasis inside the cell, which is the most influential reason of brain aging. Here, in this review, we discuss the mechanisms underneath the impairment of heat shock protein function during brain aging, including transcriptional regulation, posttranslational modification, and communication across cells and organs.
引用
收藏
页码:93 / 103
页数:11
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