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Investigation of genes coding for inflammatory components in Parkinson's disease.

Journal article
Authors Anna Håkansson
Lars Westberg
Staffan Nilsson
Silvia Buervenich
Andrea Carmine
Björn Holmberg
Olof Sydow
Lars Olson
Bo Johnels
Elias Eriksson
Hans Nissbrandt
Published in Movement disorders : official journal of the Movement Disorder Society
Volume 20
Issue 5
Pages 569-73
ISSN 0885-3185
Publication year 2005
Published at Department of Mathematical Sciences, Mathematical Statistics
Institute of Clinical Neurosciences
Institute of Physiology and Pharmacology, Dept of Pharmacology
Pages 569-73
Language en
Links dx.doi.org/10.1002/mds.20378
Keywords 1-Alkyl-2-acetylglycerophosphocholine Esterase, genetics, metabolism, Age Factors, Alleles, Brain, metabolism, Chemokine CCL2, genetics, metabolism, DNA Primers, genetics, Genotype, Humans, Inflammation, complications, genetics, metabolism, Intercellular Adhesion Molecule-1, genetics, metabolism, Interferon Type II, genetics, metabolism, Interleukin-10, genetics, metabolism, Middle Aged, Parkinson Disease, complications, genetics, metabolism, Polymorphism, Genetic, genetics, Promoter Regions (Genetics), genetics, Receptors, Interferon, genetics, metabolism, Tumor Necrosis Factor-alpha, genetics, metabolism
Subject categories Medical and Health Sciences

Abstract

Several findings obtained recently indicate that inflammation may contribute to the pathogenesis in Parkinson's disease (PD). Genetic variants of genes coding for components involved in immune reactions in the brain might therefore influence the risk of developing PD or the age of disease onset. Five single nucleotide polymorphisms (SNPs) in the genes coding for interferon-gamma (IFN-gamma; T874A in intron 1), interferon-gamma receptor 2 (IFN-gamma R2; Gln64Arg), interleukin-10 (IL-10; G1082A in the promoter region), platelet-activating factor acetylhydrolase (PAF-AH; Val379Ala), and intercellular adhesion molecule 1 (ICAM-1; Lys469Glu) were genotyped, using pyrosequencing, in 265 patients with PD and 308 controls. None of the investigated SNPs was found to be associated with PD; however, the G1082A polymorphism in the IL-10 gene promoter was found to be related to the age of disease onset. Linear regression showed a significantly earlier onset with more A-alleles (P = 0.0095; after Bonferroni correction, P = 0.048), resulting in a 5-year delayed age of onset of the disease for individuals having two G-alleles compared with individuals having two A-alleles. The results indicate that the IL-10 G1082A SNP could possibly be related to the age of onset of PD.

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