Lack of association between IL‐1β, TNF‐α, and IL‐10 gene polymorphisms and sporadic Parkinson’s disease in an Italian cohort
Identifieur interne : 000273 ( Main/Exploration ); précédent : 000272; suivant : 000274Lack of association between IL‐1β, TNF‐α, and IL‐10 gene polymorphisms and sporadic Parkinson’s disease in an Italian cohort
Auteurs : E. Pascale [Italie] ; E. Passarelli [Italie] ; C. Purcaro [Italie] ; A. R. Vestri [Italie] ; A. Fakeri [Italie] ; R. Guglielmi [Italie] ; F. Passarelli [Italie] ; G. Meco [Italie]Source :
- Acta Neurologica Scandinavica [ 0001-6314 ] ; 2011-09.
English descriptors
- KwdEn :
Abstract
Pascale E, Passarelli E, Purcaro C, Vestri AR, Fakeri A, Guglielmi R, Passarelli F, Meco G. Lack of association between IL‐1β, TNF‐α, and IL‐10 gene polymorphisms and sporadic Parkinson’s disease in an Italian cohort.
Acta Neurol Scand: 2011: 124: 176–181.
© 2010 John Wiley & Sons A/S. Objective – There is increasing evidence suggesting that neuroinflammation and microglia activation may play important roles in the pathway leading to neuronal cell death in Parkinson’s disease (PD). Chronic activation of microglia may cause neuronal damage through the release of potentially cytotoxic molecules, such as pro‐inflammatory cytokines. Different functional promoter polymorphisms within genes coding pro‐ or anti‐inflammatory cytokines involved in the immune reactions in the brain might influence the risk of developing PD or the age of disease onset. Aim – To investigate the interleukin (IL)‐1β‐511, tumor necrosis factor alpha (TNF‐α)‐308, and interleukin (IL)‐10‐1082 gene polymorphisms as susceptibility factors for PD. Methods;– We analyzed genotype and allele distributions of these polymorphisms in146 Italian patients with PD and 156 healthy controls. Results – None of the polymorphisms we investigated was found to be associated with PD or with age of disease onset. No significant differences between patients with PD and controls were found as regards the concomitant presence of variant alleles in the three polymorphisms studied. We found that only the combined genotype TNF‐α‐308GG/IL‐1β‐511T(+) is associated with a decreased risk of PD. Conclusion – Our results indicate that the cytokine gene polymorphisms we investigated are not related to the development of PD in the Italian population; further studies are warranted to clarify the role of the TNF‐α‐308GG/IL‐1β‐511T(+) combined genotype.
Url:
DOI: 10.1111/j.1600-0404.2010.01441.x
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Lack of association between IL‐1β, TNF‐α, and IL‐10 gene polymorphisms and sporadic Parkinson’s disease in an Italian cohort</title><author><name sortKey="Pascale, E" sort="Pascale, E" uniqKey="Pascale E" first="E." last="Pascale">E. Pascale</name></author><author><name sortKey="Passarelli, E" sort="Passarelli, E" uniqKey="Passarelli E" first="E." last="Passarelli">E. Passarelli</name></author><author><name sortKey="Purcaro, C" sort="Purcaro, C" uniqKey="Purcaro C" first="C." last="Purcaro">C. Purcaro</name></author><author><name sortKey="Vestri, A R" sort="Vestri, A R" uniqKey="Vestri A" first="A. R." last="Vestri">A. R. Vestri</name></author><author><name sortKey="Fakeri, A" sort="Fakeri, A" uniqKey="Fakeri A" first="A." last="Fakeri">A. Fakeri</name></author><author><name sortKey="Guglielmi, R" sort="Guglielmi, R" uniqKey="Guglielmi R" first="R." last="Guglielmi">R. Guglielmi</name></author><author><name sortKey="Passarelli, F" sort="Passarelli, F" uniqKey="Passarelli F" first="F." last="Passarelli">F. Passarelli</name></author><author><name sortKey="Meco, G" sort="Meco, G" uniqKey="Meco G" first="G." last="Meco">G. Meco</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:D15B935F6F58284DA0A45A592F5EEBCE2318E548</idno><date when="2011" year="2011">2011</date><idno type="doi">10.1111/j.1600-0404.2010.01441.x</idno><idno type="url">https://api.istex.fr/document/D15B935F6F58284DA0A45A592F5EEBCE2318E548/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">001790</idno><idno type="wicri:Area/Main/Curation">001547</idno><idno type="wicri:Area/Main/Exploration">000273</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Lack of association between IL‐1β, TNF‐α, and IL‐10 gene polymorphisms and sporadic Parkinson’s disease in an Italian cohort</title><author><name sortKey="Pascale, E" sort="Pascale, E" uniqKey="Pascale E" first="E." last="Pascale">E. Pascale</name><affiliation wicri:level="1"><country xml:lang="fr">Italie</country><wicri:regionArea>Dipartimento di Scienze e Biotecnologie Medico‐Chirurgiche, “Sapienza” Università di Roma</wicri:regionArea><wicri:noRegion>“Sapienza” Università di Roma</wicri:noRegion></affiliation></author><author><name sortKey="Passarelli, E" sort="Passarelli, E" uniqKey="Passarelli E" first="E." last="Passarelli">E. Passarelli</name><affiliation wicri:level="1"><country xml:lang="fr">Italie</country><wicri:regionArea>Dipartimento di Neurologia e Psichiatria, “Sapienza” Università di Roma</wicri:regionArea><wicri:noRegion>“Sapienza” Università di Roma</wicri:noRegion></affiliation></author><author><name sortKey="Purcaro, C" sort="Purcaro, C" uniqKey="Purcaro C" first="C." last="Purcaro">C. Purcaro</name><affiliation wicri:level="1"><country xml:lang="fr">Italie</country><wicri:regionArea>Dipartimento di Neurologia e Psichiatria, “Sapienza” Università di Roma</wicri:regionArea><wicri:noRegion>“Sapienza” Università di Roma</wicri:noRegion></affiliation></author><author><name sortKey="Vestri, A R" sort="Vestri, A R" uniqKey="Vestri A" first="A. R." last="Vestri">A. R. Vestri</name><affiliation wicri:level="1"><country xml:lang="fr">Italie</country><wicri:regionArea>Dipartimento di Sanitá Pubblica e Malattie Infettive, “Sapienza” Università di Roma</wicri:regionArea><wicri:noRegion>“Sapienza” Università di Roma</wicri:noRegion></affiliation></author><author><name sortKey="Fakeri, A" sort="Fakeri, A" uniqKey="Fakeri A" first="A." last="Fakeri">A. Fakeri</name><affiliation wicri:level="3"><country xml:lang="fr">Italie</country><wicri:regionArea>Servizio di Immunoematologia e Medicina Trasfusionale, Policlinico Umberto I, Roma</wicri:regionArea><placeName><settlement type="city">Rome</settlement><region nuts="2">Latium</region></placeName></affiliation></author><author><name sortKey="Guglielmi, R" sort="Guglielmi, R" uniqKey="Guglielmi R" first="R." last="Guglielmi">R. Guglielmi</name><affiliation wicri:level="1"><country xml:lang="fr">Italie</country><wicri:regionArea>Dipartimento di Neurologia e Psichiatria, “Sapienza” Università di Roma</wicri:regionArea><wicri:noRegion>“Sapienza” Università di Roma</wicri:noRegion></affiliation></author><author><name sortKey="Passarelli, F" sort="Passarelli, F" uniqKey="Passarelli F" first="F." last="Passarelli">F. Passarelli</name><affiliation wicri:level="1"><country xml:lang="fr">Italie</country><wicri:regionArea>Dipartimento di Medicina Molecolare, “Sapienza” Università di Roma</wicri:regionArea><wicri:noRegion>“Sapienza” Università di Roma</wicri:noRegion></affiliation></author><author><name sortKey="Meco, G" sort="Meco, G" uniqKey="Meco G" first="G." last="Meco">G. Meco</name><affiliation wicri:level="1"><country xml:lang="fr">Italie</country><wicri:regionArea>Dipartimento di Neurologia e Psichiatria, “Sapienza” Università di Roma</wicri:regionArea><wicri:noRegion>“Sapienza” Università di Roma</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Acta Neurologica Scandinavica</title><idno type="ISSN">0001-6314</idno><idno type="eISSN">1600-0404</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2011-09">2011-09</date><biblScope unit="volume">124</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="176">176</biblScope><biblScope unit="page" to="181">181</biblScope></imprint><idno type="ISSN">0001-6314</idno></series><idno type="istex">D15B935F6F58284DA0A45A592F5EEBCE2318E548</idno><idno type="DOI">10.1111/j.1600-0404.2010.01441.x</idno><idno type="ArticleID">ANE1441</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0001-6314</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>IL10</term><term>IL‐1β</term><term>Parkinson’s disease</term><term>TNF‐α</term><term>cytokine</term><term>polymorphism</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Pascale E, Passarelli E, Purcaro C, Vestri AR, Fakeri A, Guglielmi R, Passarelli F, Meco G. Lack of association between IL‐1β, TNF‐α, and IL‐10 gene polymorphisms and sporadic Parkinson’s disease in an Italian cohort.
Acta Neurol Scand: 2011: 124: 176–181.
© 2010 John Wiley & Sons A/S. Objective – There is increasing evidence suggesting that neuroinflammation and microglia activation may play important roles in the pathway leading to neuronal cell death in Parkinson’s disease (PD). Chronic activation of microglia may cause neuronal damage through the release of potentially cytotoxic molecules, such as pro‐inflammatory cytokines. Different functional promoter polymorphisms within genes coding pro‐ or anti‐inflammatory cytokines involved in the immune reactions in the brain might influence the risk of developing PD or the age of disease onset. Aim – To investigate the interleukin (IL)‐1β‐511, tumor necrosis factor alpha (TNF‐α)‐308, and interleukin (IL)‐10‐1082 gene polymorphisms as susceptibility factors for PD. Methods;– We analyzed genotype and allele distributions of these polymorphisms in146 Italian patients with PD and 156 healthy controls. Results – None of the polymorphisms we investigated was found to be associated with PD or with age of disease onset. No significant differences between patients with PD and controls were found as regards the concomitant presence of variant alleles in the three polymorphisms studied. We found that only the combined genotype TNF‐α‐308GG/IL‐1β‐511T(+) is associated with a decreased risk of PD. Conclusion – Our results indicate that the cytokine gene polymorphisms we investigated are not related to the development of PD in the Italian population; further studies are warranted to clarify the role of the TNF‐α‐308GG/IL‐1β‐511T(+) combined genotype.</div></front></TEI><affiliations><list><country><li>Italie</li></country><region><li>Latium</li></region><settlement><li>Rome</li></settlement></list><tree><country name="Italie"><noRegion><name sortKey="Pascale, E" sort="Pascale, E" uniqKey="Pascale E" first="E." last="Pascale">E. Pascale</name></noRegion><name sortKey="Fakeri, A" sort="Fakeri, A" uniqKey="Fakeri A" first="A." last="Fakeri">A. Fakeri</name><name sortKey="Guglielmi, R" sort="Guglielmi, R" uniqKey="Guglielmi R" first="R." last="Guglielmi">R. Guglielmi</name><name sortKey="Meco, G" sort="Meco, G" uniqKey="Meco G" first="G." last="Meco">G. Meco</name><name sortKey="Passarelli, E" sort="Passarelli, E" uniqKey="Passarelli E" first="E." last="Passarelli">E. Passarelli</name><name sortKey="Passarelli, F" sort="Passarelli, F" uniqKey="Passarelli F" first="F." last="Passarelli">F. Passarelli</name><name sortKey="Purcaro, C" sort="Purcaro, C" uniqKey="Purcaro C" first="C." last="Purcaro">C. Purcaro</name><name sortKey="Vestri, A R" sort="Vestri, A R" uniqKey="Vestri A" first="A. R." last="Vestri">A. R. Vestri</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000273 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000273 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= ISTEX:D15B935F6F58284DA0A45A592F5EEBCE2318E548
|texte= Lack of association between IL‐1β, TNF‐α, and IL‐10 gene polymorphisms and sporadic Parkinson’s disease in an Italian cohort
}}
| This area was generated with Dilib version V0.6.23. |  |