Age-dependent accumulation of oligomeric SNCA/α-synuclein from impaired degradation in mutant LRRK2 knockin mouse model of Parkinson disease: role for therapeutic activation of chaperone-mediated autophagy (CMA)-Reference-Cited by-同舟云学术

Age-dependent accumulation of oligomeric SNCA/α-synuclein from impaired degradation in mutant LRRK2 knockin mouse model of Parkinson disease: role for therapeutic activation of chaperone-mediated autophagy (CMA)

Published:2019-04-14 Issue:2 Volume:16 Page:347-370
ISSN:1554-8627
Container-title:Autophagy
language:en
Short-container-title:Autophagy

Author:

Ho Philip Wing-Lok¹^ORCID,Leung Chi-Ting¹,Liu Huifang¹,Pang Shirley Yin-Yu¹,Lam Colin Siu-Chi¹,Xian Jiawen¹,Li Lingfei¹,Kung Michelle Hiu-Wai¹,Ramsden David Boyer²^ORCID,Ho Shu-Leong¹^ORCID

Affiliation:

1. Division of Neurology, Department of Medicine, University of Hong Kong, Queen Mary Hospital , Hong Kong S.A.R., China

2. Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK

Funder

JABBS Charity

Health and Medical Research Fund

Tai Hung Fai Charitable Foundation - Edwin S H Leong Research Programme for Parkinson’s Disease

Publisher

Informa UK Limited

Subject

Cell Biology,Molecular Biology

Link

https://www.tandfonline.com/doi/pdf/10.1080/15548627.2019.1603545

Reference85 articles.

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2. Parkinson's disease: from monogenic forms to genetic susceptibility factors

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4. Progress in unraveling the genetic etiology of Parkinson disease in a genomic era

5. Genome-wide association study identifies common variants at four loci as genetic risk factors for Parkinson's disease

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