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Supportive evidence for 11 loci from genome-wide association studies in Parkinson's disease

Journal article
Authors L. Pihlstrom
G. Axelsson
K. A. Bjornara
N. Dizdar
Camilla Fardell
L. Forsgren
Björn Holmberg
J. P. Larsen
J. Linder
Hans Nissbrandt
O. B. Tysnes
E. Ohman
E. Dietrichs
M. Toft
Published in Neurobiology of Aging
Volume 34
Issue 6
Pages Article Number: 1708.e7
ISSN 0197-4580
Publication year 2013
Published at Institute of Neuroscience and Physiology
Institute of Neuroscience and Physiology, Department of Pharmacology
Pages Article Number: 1708.e7
Language en
Links dx.doi.org/10.1016/j.neurobiolaging...
Keywords Parkinson's disease, GWAS, Genetic association study, Single-nucleotide polymorphism, risk-factors, identification, metaanalysis, population, variants, genetics, linkage, region, snca, hla, DC62/HIP1R, SYT11, GAK, STX1B, MCCC1/LAMP3, ACMSD, and FGF20). The more recently nominated
Subject categories Geriatrics, Neurology

Abstract

enome-wide association studies have identified a number of susceptibility loci in sporadic Parkinson's disease (PD). Recent larger studies and meta-analyses have greatly expanded the list of proposed association signals. We performed a case-control replication study in a Scandinavian population, analyzing samples from 1345 unrelated PD patients and 1225 control subjects collected by collaborating centers in Norway and Sweden. Single-nucleotide polymorphisms representing 18 loci previously reported at genome-wide significance levels were genotyped, as well as 4 near-significant, suggestive, loci. We replicated 11 association signals at p < 0.05 (SNCA, STK39, MAPT, GPNMB, CCDC62/HIP1R, SYT11, GAK, STX1B, MCCC1/LAMP3, ACMSD, and FGF20). The more recently nominated susceptibility loci were well represented among our positive findings, including 3 which have not previously been validated in independent studies. Conversely, some of the more well-established loci failed to replicate. While future meta-analyses should corroborate disease associations further on the level of common markers, efforts to pinpoint functional variants and understand the biological implications of each risk locus in PD are also warranted.

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