Lowering mutant huntingtin levels and toxicity: autophagy-endolysosome pathways in Huntington’s disease.

Lowering mutant huntingtin levels and toxicity: autophagy-endolysosome pathways in Huntington’s disease.

Publication date: Nov 28, 2019

Huntington’s disease 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 Huntington’s disease. 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.

Valionyte, E., Yang, Y., Roberts, S.L., Kelly, J., Lu, B., and Luo, S. Lowering mutant huntingtin levels and toxicity: autophagy-endolysosome pathways in Huntington’s disease. 06806. 2019 J Mol Biol.

Concepts Keywords
Autophagy Monogenetic neurodegenerative disease
Endolysosome Branches of biology
Flux Cellular processes
Huntingtin Programmed cell death
Huntington Autophagy
Mutant Immunology
Neurodegeneration Neurodegeneration
Neurodegenerative Disease MTOR
Neurodegenerative Diseases Huntingtin
Neurodegenerative Disorders Huntington’s disease
Pathology
Restoration
Toxicity

Semantics

Type Source Name
disease MESH pathology
disease MESH neurodegenerative disease
pathway KEGG Autophagy

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