Autophagy impairment in Parkinson’s disease

Author:

Karabiyik Cansu1,Lee Min Jae2,Rubinsztein David C.13

Affiliation:

1. Department of Medical Genetics, Cambridge Institute for Medical Research, Cambridge Biomedical Campus, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0XY, U.K.

2. Department of Biochemistry and Molecular Biology, Seoul National University College of Medicine, Seoul 03080, Korea

3. UK Dementia Research Institute, Cambridge Biomedical Campus, Cambridge Biomedical Campus, Hills Road, Cambridge, U.K.

Abstract

Parkinson’s disease (PD) is a debilitating movement disorder typically associated with the accumulation of intracytoplasmic aggregate prone protein deposits. Over recent years, increasing evidence has led to the suggestion that the mutations underlying certain forms of PD impair autophagy. Autophagy is a degradative pathway that delivers cytoplasmic content to lysosomes for degradation and represents a major route for degradation of aggregated cellular proteins and dysfunctional organelles. Autophagy up-regulation is a promising therapeutic strategy that is being explored for its potential to protect cells against the toxicity of aggregate-prone proteins in neurodegenerative diseases. Here, we describe how the mutations in different subtypes of PD can affect different stages of autophagy.

Publisher

Portland Press Ltd.

Subject

Molecular Biology,Biochemistry

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