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LAMP2A as a therapeutic target in Parkinson disease

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Author

  • Maria Xilouri
  • Oeystein Roed Brekk
  • Deniz Kirik
  • Leonidas Stefanis

Summary, in English

Abnormal aggregation of SNCA/-synuclein plays a crucial role in Parkinson disease (PD) pathogenesis. SNCA levels determine its toxicity, and its accumulation, even to a small extent, may be a risk factor for neurodegeneration. One of the main pathways for SNCA degradation is chaperone-mediated autophagy (CMA), a selective form of autophagy, while aberrant SNCA may act as a CMA inhibitor. In the current punctum we summarize our recent data showing that induction of CMA, via overexpression of the protein controlling its rate-limiting step, the lysosomal receptor LAMP2A, effectively decreases SNCA levels and ameliorates SNCA-induced neurodegeneration, both in neuronal cell culture systems and in the rat brain. Such findings suggest that modulation of LAMP2A and, consequently, CMA, represents a viable therapeutic target for PD and other synucleinopathies where SNCA accumulation and aggregation plays a fundamental role.

Publishing year

2013

Language

English

Pages

2166-2168

Publication/Series

Autophagy

Volume

9

Issue

12

Document type

Journal article (comment)

Publisher

Landes Bioscience

Topic

  • Cell and Molecular Biology

Keywords

  • alpha-synuclein
  • chaperone-mediated autophagy
  • dopaminergic system
  • LAMP2A
  • neurotoxicity
  • Parkinson disease
  • substantia nigra

Status

Published

Research group

  • Brain Repair and Imaging in Neural Systems (BRAINS)

ISBN/ISSN/Other

  • ISSN: 1554-8635