@article{3da926cb2df34114b2a0a781d5306387,
title = "Lowering Mutant Huntingtin Levels and Toxicity: Autophagy-Endolysosome Pathways in Huntington's Disease",
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.",
keywords = "Autophagy, Huntingtin, Huntington's disease, Neurodegeneration, Selective autophagy",
author = "Evelina Valionyte and Yi Yang and Roberts, {Sheridan L.} and Jack Kelly and Boxun Lee and Shouqing Luo",
note = "Funding Information: The authors are grateful to the Medical Research Council UK ( MR/M023605/1 ), the UK Academy of Medical Sciences and Newton Fund for Newton Advanced Fellowship ( NAF∖R1∖191045 ), and the National Natural Science Foundation of China ( 91649105 ) for funding. Funding Information: The authors are grateful to the Medical Research Council UK (MR/M023605/1), the UK Academy of Medical Sciences and Newton Fund for Newton Advanced Fellowship (NAF?R1?191045), and the National Natural Science Foundation of China (91649105) for funding. Publisher Copyright: {\textcopyright} 2019 Elsevier Ltd",
year = "2020",
month = apr,
day = "3",
doi = "10.1016/j.jmb.2019.11.012",
language = "English",
volume = "432",
pages = "2673--2691",
journal = "Journal of molecular biology",
issn = "0022-2836",
publisher = "Academic Press",
number = "8",
}