期刊
CURRENT NEUROPHARMACOLOGY
卷 14, 期 3, 页码 238-249出版社
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1570159X13666151030103027
关键词
Parkinson's disease; autophagy; alpha-synuclein; LRRK2; lysosome; mTOR; rapamycin; TFEB
资金
- FEDER
- Spanish Ministry of Economy and Competitiveness [SAF2014-58653-R]
- Junta de Andalucia [CTS-6816]
- BBVA Foundation
- Michael J. Fox Foundation
- Juan de la Cierva Fellowship (MINECO) [JCI2010-07703]
- FEDER
- Spanish Ministry of Economy and Competitiveness [SAF2014-58653-R]
- Junta de Andalucia [CTS-6816]
- BBVA Foundation
- Michael J. Fox Foundation
- Juan de la Cierva Fellowship (MINECO) [JCI2010-07703]
Autophagy is a cellular quality control mechanism crucial for neuronal homeostasis. Defects in autophagy are critically associated with mechanisms underlying Parkinson's disease (PD), a common and debilitating neurodegenerative disorder. Autophagic dysfunction in PD can occur at several stages of the autophagy/lysosomal degradative machinery, contributing to the formation of intracellular protein aggregates and eventual neuronal cell death. Therefore, autophagy inducers may comprise a promising new therapeutic approach to combat neurodegeneration in PD. Several currently available FDA-approved drugs have been shown to enhance autophagy, which may allow for their repurposing for use in novel clinical conditions including PD. This review summarizes our current knowledge of deficits in the autophagy/lysosomal degradation pathways associated with PD, and highlight current approaches which target this pathway as possible means towards novel therapeutic strategies.
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