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LAMP2A as a therapeutic target in Parkinson disease

Xilouri, Maria ; Brekk, Oeystein Roed ; Kirik, Deniz LU and Stefanis, Leonidas (2013) In Autophagy 9(12). p.2166-2168
Abstract
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... (More)
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. (Less)
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author
; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
alpha-synuclein, chaperone-mediated autophagy, dopaminergic system, LAMP2A, neurotoxicity, Parkinson disease, substantia nigra
in
Autophagy
volume
9
issue
12
pages
2166 - 2168
publisher
Landes Bioscience
external identifiers
  • wos:000328299800023
  • scopus:84890829178
  • pmid:24145820
ISSN
1554-8635
DOI
10.4161/auto.26451
language
English
LU publication?
yes
id
597193b7-99ff-4062-af28-57fea0d68af2 (old id 4269033)
date added to LUP
2016-04-01 09:49:29
date last changed
2022-04-27 07:44:58
@misc{597193b7-99ff-4062-af28-57fea0d68af2,
  abstract     = {{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.}},
  author       = {{Xilouri, Maria and Brekk, Oeystein Roed and Kirik, Deniz and Stefanis, Leonidas}},
  issn         = {{1554-8635}},
  keywords     = {{alpha-synuclein; chaperone-mediated autophagy; dopaminergic system; LAMP2A; neurotoxicity; Parkinson disease; substantia nigra}},
  language     = {{eng}},
  number       = {{12}},
  pages        = {{2166--2168}},
  publisher    = {{Landes Bioscience}},
  series       = {{Autophagy}},
  title        = {{LAMP2A as a therapeutic target in Parkinson disease}},
  url          = {{http://dx.doi.org/10.4161/auto.26451}},
  doi          = {{10.4161/auto.26451}},
  volume       = {{9}},
  year         = {{2013}},
}