Protein clearance mechanisms and their demise in age-related neurodegenerative diseases

AIMS Molecular Science

Isabel Saez¹  David Vilchez¹ 

[1] Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Joseph Stelzmann Strasse 26, 50931 Cologne, Germany;

关键词: proteostasis;    ageing;    neurodegeneration;    proteasome;    autophagy;   

DOI  :  10.3934/molsci.2015.1.1

来源: DOAJ

【 摘 要 】

The accumulation of damaged proteins contributes to the etiology of neurodegenerative diseases such as Alzheimer’s, Parkinson’s, Huntington’s or amyotrophic lateral sclerosis. Protein aggregation and deposition are common features of these disorders that share emergence patterns and are more frequent late in life, even though different toxic proteins are involved in their onset. The ability to maintain a functional proteome, or proteostasis, declines during the ageing process. Damaged proteins are degraded by the ubiquitin proteasome system or through autophagy-lysosome, key components of the proteostasis network. Here we review the links between neurodegenerative disorders and loss of protein clearance mechanisms with age.

【 授权许可】

Unknown