Funding agencies: This study was supported by Kompetenznetz Parkinson (BMB+F: 01GI0201).
Article first published online: 2 AUG 2011
Copyright © 2011 Movement Disorder Society
Volume 26, Issue 13, pages 2415–2417, November 2011
How to Cite
Kauther, K. M., Höft, C., Rissling, I., Oertel, W. H. and Möller, J. C. (2011), The PLA2G6 gene in early-onset Parkinson's disease. Mov. Disord., 26: 2415–2417. doi: 10.1002/mds.23851
Relevant conflicts of interest/financial disclosures: Nothing to report.
Full financial disclosures and author roles may be found in the online version of this article.
- Issue published online: 22 NOV 2011
- Article first published online: 2 AUG 2011
- Manuscript Accepted: 26 MAY 2011
- Manuscript Revised: 24 APR 2011
- Manuscript Received: 25 MAY 2010
- Parkinson syndrome;
The definite etiology of neurodegenerative disorders such as Parkinson's disease (PD) is still unknown. Because of its role in the generation of reactive oxygen species and its association with neurodegeneration with brain iron accumulation, a possible involvement of calcium-independent group VI phospholipase A2 (iPLA2-VI) in the pathogenesis of PD has been proposed.
In this study we analyzed all 17 exons of the PLA2G6 gene encoding iPLA2-VI in a group of 102 discordant pairs with early-onset Parkinson's disease (EOPD) and an additional sample of 166 EOPD patients and 155 unrelated controls.
The nonsynonymous single-nucleotide polymorphisms (SNPs) 2339A>G (n = 2) and 2341G>A (n = 1) in 2 neighboring codons were found in 3 patients with typical L-dopa-responsive sporadic EOPD and in none of our controls, indicating a possible role of PLA2G6 in the pathogenesis of EOPD in rare cases.
Future studies should investigate the prevalence of these SNPs in other PD populations and larger control groups and also address possible genetic alterations in the remaining parts of the PLA2G6 gene. © 2011 Movement Disorder Society