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Updated: Sep 17, 2025

Studies of Chaperone-Cochaperone Interactions using Homogenous Bead-Based Assay
Published on: July 21, 2021
Chaperone-Mediated Autophagy: A Critical Regulator of Neuroinflammation and Neurodegeneration
Ying-Ying Han1,2, Xin-Yue Huang2, Ying Su1
1Department of Pharmacy, The Fourth Affiliated Hospital of Soochow University, Suzhou Dushu Lake Hospital, Medical Center of Soochow University, Suzhou, 215123, China.
Abstract:
Neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD), are characterized by hallmark pathological features such as the accumulation of misfolded proteins and neuroinflammation. Chaperone-mediated autophagy (CMA), a selective lysosomal pathway, facilitates the degradation of proteins containing KFERQ-like motifs via the receptor lysosome-associated membrane protein type 2A (LAMP2A). In the recent review, the pivotal role of CMA in regulating proteostasis and modulating inflammatory responses is highlighted. This commentary explores the multifaceted roles of CMA in neurodegenerative disease progression, emphasizing its involvement in age-related decline, feedback loops between CMA dysregulation and neurodegeneration, and potential as a therapeutic target. Emerging CMA activators and the challenges of modulating CMA for clinical use are also discussed.
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