Chaperone-mediated autophagy and neurodegeneration: connections, mechanisms, and therapeutic implications.

Abstract

Lysosomes degrade dysfunctional intracellular components via three pathways: macroautophagy, microautophagy, and chaperone-mediated autophagy (CMA). Unlike the other two, CMA degrades cytosolic proteins with a recognized KFERQ-like motif in lysosomes and is important for cellular homeostasis. CMA activity declines with age and is altered in neurodegenerative diseases. Its impairment leads to the accumulation of aggregated proteins, some of which may be directly tied to the pathogenic processes of neurodegenerative diseases. Its induction may accelerate the clearance of pathogenic proteins and promote cell survival, representing a potential therapeutic approach for the treatment of neurodegenerative diseases. In this review, we summarize the current findings on how CMA is involved in neurodegenerative diseases, especially in Parkinson's disease.

• Authors: Xiaolei Liu, Sihua Huang, Xingqin Wang, Beisha Tang, Wenming Li, Zixu Mao
• Journal: Neuroscience bulletin (Neurosci Bull) Vol. 31 Issue 4 Pg. 407-15 (Aug 2015) ISSN: 1995-8218 [Electronic] Singapore
• PMID: 26206600 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Review)

Chemical References

• Molecular Chaperones

Topics

• Animals
• Autophagy
• Brain (metabolism, physiopathology)
• Humans
• Lysosomes (metabolism, physiology)
• Molecular Chaperones
• Neurodegenerative Diseases (metabolism, physiopathology, therapy)