Format

Send to

Choose Destination
Mol Neurobiol. 2015 Feb;51(1):89-104. doi: 10.1007/s12035-014-8787-5. Epub 2014 Jul 4.

Defective autophagy in Parkinson's disease: lessons from genetics.

Author information

1
Center of Parkinson's Disease Beijing Institute for Brain Disorders, Key Laboratory for Neurodegenerative Disease of the Ministry of Education, Department of Neurobiology Capital Medical University, Beijing, 100069, China.

Abstract

Parkinson's disease (PD) is the most prevalent neurodegenerative movement disorder. Genetic studies over the past two decades have greatly advanced our understanding of the etiological basis of PD and elucidated pathways leading to neuronal degeneration. Recent studies have suggested that abnormal autophagy, a well conserved homeostatic process for protein and organelle turnover, may contribute to neurodegeneration in PD. Moreover, many of the proteins related to both autosomal dominant and autosomal recessive PD, such as α-synuclein, PINK1, Parkin, LRRK2, DJ-1, GBA, and ATPA13A2, are also involved in the regulation of autophagy. We propose that reduced autophagy enhances the accumulation of α-synuclein, other pathogenic proteins, and dysfunctional mitochondria in PD, leading to oxidative stress and neuronal death.

PMID:
24990317
DOI:
10.1007/s12035-014-8787-5
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center