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NURR1 in Parkinson disease-from pathogenesis to therapeutic potential.

Decressac, Mickael LU ; Volakakis, Nikolaos; Björklund, Anders LU and Perlmann, Thomas (2013) In Nature Reviews Neurology 9(11). p.629-636
Abstract
In Parkinson disease (PD), affected midbrain dopamine (DA) neurons lose specific dopaminergic properties before the neurons die. How the phenotype of DA neurons is normally established and the ways in which pathology affects the maintenance of cell identity are, therefore, important considerations. Orphan nuclear receptor NURR1 (NURR1, also known as NR4A2) is involved in the differentiation of midbrain DA neurons, but also has an important role in the adult brain. Emerging evidence indicates that impaired NURR1 function might contribute to the pathogenesis of PD: NURR1 and its transcriptional targets are downregulated in midbrain DA neurons that express high levels of the disease-causing protein α-synuclein. Clinical and experimental data... (More)
In Parkinson disease (PD), affected midbrain dopamine (DA) neurons lose specific dopaminergic properties before the neurons die. How the phenotype of DA neurons is normally established and the ways in which pathology affects the maintenance of cell identity are, therefore, important considerations. Orphan nuclear receptor NURR1 (NURR1, also known as NR4A2) is involved in the differentiation of midbrain DA neurons, but also has an important role in the adult brain. Emerging evidence indicates that impaired NURR1 function might contribute to the pathogenesis of PD: NURR1 and its transcriptional targets are downregulated in midbrain DA neurons that express high levels of the disease-causing protein α-synuclein. Clinical and experimental data indicate that disrupted NURR1 function contributes to induction of DA neuron dysfunction, which is seen in early stages of PD. The likely involvement of NURR1 in the development and progression of PD makes this protein a potentially interesting target for therapeutic intervention. (Less)
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Contribution to journal
publication status
published
subject
in
Nature Reviews Neurology
volume
9
issue
11
pages
629 - 636
publisher
Nature Publishing Group
external identifiers
  • wos:000329215900009
  • pmid:24126627
  • scopus:84887257119
ISSN
1759-4766
DOI
10.1038/nrneurol.2013.209
language
English
LU publication?
yes
id
321a286c-e4c7-4407-b990-fad09952e9ca (old id 4143246)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/24126627?dopt=Abstract
date added to LUP
2013-11-05 00:14:36
date last changed
2019-04-21 03:03:49
@article{321a286c-e4c7-4407-b990-fad09952e9ca,
  abstract     = {In Parkinson disease (PD), affected midbrain dopamine (DA) neurons lose specific dopaminergic properties before the neurons die. How the phenotype of DA neurons is normally established and the ways in which pathology affects the maintenance of cell identity are, therefore, important considerations. Orphan nuclear receptor NURR1 (NURR1, also known as NR4A2) is involved in the differentiation of midbrain DA neurons, but also has an important role in the adult brain. Emerging evidence indicates that impaired NURR1 function might contribute to the pathogenesis of PD: NURR1 and its transcriptional targets are downregulated in midbrain DA neurons that express high levels of the disease-causing protein α-synuclein. Clinical and experimental data indicate that disrupted NURR1 function contributes to induction of DA neuron dysfunction, which is seen in early stages of PD. The likely involvement of NURR1 in the development and progression of PD makes this protein a potentially interesting target for therapeutic intervention.},
  author       = {Decressac, Mickael and Volakakis, Nikolaos and Björklund, Anders and Perlmann, Thomas},
  issn         = {1759-4766},
  language     = {eng},
  number       = {11},
  pages        = {629--636},
  publisher    = {Nature Publishing Group},
  series       = {Nature Reviews Neurology},
  title        = {NURR1 in Parkinson disease-from pathogenesis to therapeutic potential.},
  url          = {http://dx.doi.org/10.1038/nrneurol.2013.209},
  volume       = {9},
  year         = {2013},
}