Investigation of genes coding for inflammatory components in Parkinson's disease
Identifieur interne : 002216 ( Main/Curation ); précédent : 002215; suivant : 002217Investigation of genes coding for inflammatory components in Parkinson's disease
Auteurs : Anna H Kansson [Suède] ; Lars Westberg [Suède] ; Staffan Nilsson [Suède] ; Silvia Buervenich [Suède] ; Andrea Carmine [Suède] ; Björn Holmberg [Suède] ; Olof Sydow [Suède] ; Lars Olson [Suède] ; Bo Johnels [Suède] ; Elias Eriksson [Suède] ; Hans Nissbrandt [Suède]Source :
- Movement Disorders [ 0885-3185 ] ; 2005-05.
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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‐γ (IFN‐γ; T874A in intron 1), interferon‐γ receptor 2 (IFN‐γ 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. © 2005 Movement Disorder Society
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DOI: 10.1002/mds.20378
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Göteborg</wicri:regionArea></affiliation></author><author><name sortKey="Eriksson, Elias" sort="Eriksson, Elias" uniqKey="Eriksson E" first="Elias" last="Eriksson">Elias Eriksson</name><affiliation wicri:level="1"><mods:affiliation>Department of Pharmacology, Sahlgrenska Academy at Göteborg University, Göteborg, Sweden</mods:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Pharmacology, Sahlgrenska Academy at Göteborg University, Göteborg</wicri:regionArea></affiliation></author><author><name sortKey="Nissbrandt, Hans" sort="Nissbrandt, Hans" uniqKey="Nissbrandt H" first="Hans" last="Nissbrandt">Hans Nissbrandt</name><affiliation wicri:level="1"><mods:affiliation>Department of Pharmacology, Sahlgrenska Academy at Göteborg University, Göteborg, Sweden</mods:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Pharmacology, Sahlgrenska Academy at Göteborg University, Göteborg</wicri:regionArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2005-05">2005-05</date><biblScope unit="volume">20</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="569">569</biblScope><biblScope unit="page" to="573">573</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">572F160E7E2221C0D070F5627730F9C2E6FAC533</idno><idno type="DOI">10.1002/mds.20378</idno><idno type="ArticleID">MDS20378</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>intercellular adhesion molecule 1</term><term>interferon‐γ</term><term>interferon‐γ receptor 2</term><term>interleukin‐10</term><term>platelet‐activating factor acetylhydrolase</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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‐γ (IFN‐γ; T874A in intron 1), interferon‐γ receptor 2 (IFN‐γ 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. © 2005 Movement Disorder Society</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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