Lowering Mutant Huntingtin Levels and Toxicity: Autophagy-Endolysosome Pathways in Huntington's Disease

Research output: Contribution to journalReview articlepeer-review

  • External authors:
  • Evelina Valionyte (Lead)
  • Yi Yang
  • Sheridan L. Roberts
  • Boxun Lee
  • Shouqing Luo

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.

Bibliographical metadata

Original languageEnglish
Pages (from-to)2673-2691
Number of pages19
JournalJournal of molecular biology
Volume432
Issue number8
DOIs
Publication statusPublished - 3 Apr 2020