Chaperone-mediated autophagy: Roles in neurodegeneration

• Type of Material: Article
• Authors: Gang Wang, Emory University; Zixu Mao, Emory University
• Language: English
• Date: 2014-09-21
• Publisher: BioMed Central Ltd.
• Publication Version: Final Published Version
• Copyright Statement: © 2014 Wang and Mao; licensee BioMed Central Ltd.
• Final Published Version (URL): http://dx.doi.org/10.1186/2047-9158-3-20
• Title of Journal or Parent Work: Translational Neurodegeneration
• Volume: 3
• Issue: 1
• Start Page: 20
• End Page: 20
• Grant/Funding Information: This work was in part supported by grants to Z.M (NIH AG023695, NS079858, and ES015317). We thank Dr. Eric B. Dammer in department of Biochemistry, Emory University School of Medicine, Atlanta for proof reading.
• Keywords: Parkinson's disease; Chaperone-mediated autophagy; Protein posttranslational modifications; Alzheimer's disease; Neurodegeneration
• Research Categories: Health Sciences, Public Health; Health Sciences, Pharmacology; Health Sciences, General

Abstract

Chaperone-mediated autophagy (CMA) selectively delivers cytosolic proteins with an exposed CMA-targeting motif to lysosomes for degradation and plays an important role in protein quality control and cellular homeostasis. A growing body of evidence supports the hypothesis that CMA dysfunction may be involved in the pathogenic process of neurodegenerative diseases. Both down-regulation and compensatory up-regulation in CMA activities have been observed in association with neurodegenerative conditions. Recent studies have revealed several new mechanisms by which CMA function may be involved in the regulation of factors critical for neuronal viability and homeostasis. Here, we summarize these recent advances in the understanding of the relationship between CMA dysfunction and neurodegeneration and discuss the therapeutic potential of targeting CMA in the treatment of neurodegenerative diseases.