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Updated: Jan 2, 2026

Fractionation for Resolution of Soluble and Insoluble Huntingtin Species
Published on: February 27, 2018
Lowering Mutant Huntingtin Levels and Toxicity: Autophagy-Endolysosome Pathways in Huntington's Disease
Evelina Valionyte1, Yi Yang1, Sheridan L Roberts1
1Peninsula Schools of Medicine and Dentistry, Institute of Translational and Stratified Medicine, University of Plymouth, Research Way, Plymouth PL6 8BU, UK.
Abstract:
Huntington's disease (HD) is a monogenetic neurodegenerative disease, which serves as a model of neurodegeneration with protein aggregation. Autophagy has been suggested to possess a great value to tackle protein aggregation toxicity and neurodegenerative diseases. Current studies suggest that autophagy-endolysosomal pathways are critical for HD pathology. Here we review recent advancement in the studies of autophagy and selective autophagy relating HD. Restoration of autophagy flux and enhancement of selective removal of mutant huntingtin/disease-causing protein would be effective approaches towards tackling HD as well as other similar neurodegenerative disorders.
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