LAMP2A as a therapeutic target in Parkinson disease
Författare
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.
Avdelning/ar
Publiceringsår
2013
Språk
Engelska
Sidor
2166-2168
Publikation/Tidskrift/Serie
Autophagy
Volym
9
Issue
12
Dokumenttyp
Artikel i tidskrift
Förlag
Landes Bioscience
Ämne
- Cell and Molecular Biology
Nyckelord
- alpha-synuclein
- chaperone-mediated autophagy
- dopaminergic system
- LAMP2A
- neurotoxicity
- Parkinson disease
- substantia nigra
Status
Published
Forskningsgrupp
- Brain Repair and Imaging in Neural Systems (BRAINS)
ISBN/ISSN/Övrigt
- ISSN: 1554-8635