Complex interactions in Parkinson's disease: a two-phased approach.
Identifieur interne : 000A73 ( Ncbi/Curation ); précédent : 000A72; suivant : 000A74Complex interactions in Parkinson's disease: a two-phased approach.
Auteurs : Demetrius M. Maraganore [États-Unis] ; Mariza De Andrade ; Timothy G. Lesnick ; Matthew J. Farrer ; James H. Bower ; John A. Hardy ; Walter A. RoccaSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2003.
English descriptors
- KwdEn :
- Case-Control Studies, DNA Restriction Enzymes, Female, Genetic Predisposition to Disease, Genotype, Humans, Ligases (genetics), Logistic Models, Male, Movement Disorders (genetics), Mutation, Nerve Tissue Proteins (genetics), Parkinson Disease (genetics), Polymerase Chain Reaction (methods), Synucleins, Thiolester Hydrolases (genetics), Ubiquitin Thiolesterase, Ubiquitin-Protein Ligases, alpha-Synuclein.
- MESH :
- chemical , genetics : Ligases, Nerve Tissue Proteins, Thiolester Hydrolases.
- chemical : DNA Restriction Enzymes, Synucleins, Ubiquitin Thiolesterase, Ubiquitin-Protein Ligases, alpha-Synuclein.
- genetics : Movement Disorders, Parkinson Disease.
- methods : Polymerase Chain Reaction.
- Case-Control Studies, Female, Genetic Predisposition to Disease, Genotype, Humans, Logistic Models, Male, Mutation.
Abstract
The identification of pathogenic mutations in the three genes alpha-synuclein, parkin, and ubiquitin carboxy-terminal hydrolase L1 (UCHL1) has elucidated the ubiquitin proteasome system (UPS) and its potential role as a causal pathway in Parkinson's disease (PD). In addition, polymorphisms of these three genes have been shown to be independently associated with PD. In a sample of 298 unrelated PD cases and 185 controls, we applied a two-phased approach of recursive partitioning and logistic regression analyses to explore complex interactions. For women only, we observed an epistatic interaction of UCHL1 and alpha-synuclein genotypes with significant effects on PD risk (odds ratio = 2.42; P = 0.003). Our findings are consistent with the hypothesis that PD is a multigenic disorder of the UPS.
DOI: 10.1002/mds.10431
PubMed: 12784265
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Complex interactions in Parkinson's disease: a two-phased approach.</title><author><name sortKey="Maraganore, Demetrius M" sort="Maraganore, Demetrius M" uniqKey="Maraganore D" first="Demetrius M" last="Maraganore">Demetrius M. Maraganore</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905, USA. dmaraganore@mayo.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905</wicri:regionArea><wicri:noRegion>Minnesota 55905</wicri:noRegion></affiliation></author><author><name sortKey="De Andrade, Mariza" sort="De Andrade, Mariza" uniqKey="De Andrade M" first="Mariza" last="De Andrade">Mariza De Andrade</name></author><author><name sortKey="Lesnick, Timothy G" sort="Lesnick, Timothy G" uniqKey="Lesnick T" first="Timothy G" last="Lesnick">Timothy G. Lesnick</name></author><author><name sortKey="Farrer, Matthew J" sort="Farrer, Matthew J" uniqKey="Farrer M" first="Matthew J" last="Farrer">Matthew J. Farrer</name></author><author><name sortKey="Bower, James H" sort="Bower, James H" uniqKey="Bower J" first="James H" last="Bower">James H. Bower</name></author><author><name sortKey="Hardy, John A" sort="Hardy, John A" uniqKey="Hardy J" first="John A" last="Hardy">John A. Hardy</name></author><author><name sortKey="Rocca, Walter A" sort="Rocca, Walter A" uniqKey="Rocca W" first="Walter A" last="Rocca">Walter A. 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Maraganore</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905, USA. dmaraganore@mayo.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905</wicri:regionArea><wicri:noRegion>Minnesota 55905</wicri:noRegion></affiliation></author><author><name sortKey="De Andrade, Mariza" sort="De Andrade, Mariza" uniqKey="De Andrade M" first="Mariza" last="De Andrade">Mariza De Andrade</name></author><author><name sortKey="Lesnick, Timothy G" sort="Lesnick, Timothy G" uniqKey="Lesnick T" first="Timothy G" last="Lesnick">Timothy G. Lesnick</name></author><author><name sortKey="Farrer, Matthew J" sort="Farrer, Matthew J" uniqKey="Farrer M" first="Matthew J" last="Farrer">Matthew J. Farrer</name></author><author><name sortKey="Bower, James H" sort="Bower, James H" uniqKey="Bower J" first="James H" last="Bower">James H. Bower</name></author><author><name sortKey="Hardy, John A" sort="Hardy, John A" uniqKey="Hardy J" first="John A" last="Hardy">John A. Hardy</name></author><author><name sortKey="Rocca, Walter A" sort="Rocca, Walter A" uniqKey="Rocca W" first="Walter A" last="Rocca">Walter A. Rocca</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2003" type="published">2003</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Case-Control Studies</term><term>DNA Restriction Enzymes</term><term>Female</term><term>Genetic Predisposition to Disease</term><term>Genotype</term><term>Humans</term><term>Ligases (genetics)</term><term>Logistic Models</term><term>Male</term><term>Movement Disorders (genetics)</term><term>Mutation</term><term>Nerve Tissue Proteins (genetics)</term><term>Parkinson Disease (genetics)</term><term>Polymerase Chain Reaction (methods)</term><term>Synucleins</term><term>Thiolester Hydrolases (genetics)</term><term>Ubiquitin Thiolesterase</term><term>Ubiquitin-Protein Ligases</term><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Ligases</term><term>Nerve Tissue Proteins</term><term>Thiolester Hydrolases</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>DNA Restriction Enzymes</term><term>Synucleins</term><term>Ubiquitin Thiolesterase</term><term>Ubiquitin-Protein Ligases</term><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Movement Disorders</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Polymerase Chain Reaction</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Case-Control Studies</term><term>Female</term><term>Genetic Predisposition to Disease</term><term>Genotype</term><term>Humans</term><term>Logistic Models</term><term>Male</term><term>Mutation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The identification of pathogenic mutations in the three genes alpha-synuclein, parkin, and ubiquitin carboxy-terminal hydrolase L1 (UCHL1) has elucidated the ubiquitin proteasome system (UPS) and its potential role as a causal pathway in Parkinson's disease (PD). In addition, polymorphisms of these three genes have been shown to be independently associated with PD. In a sample of 298 unrelated PD cases and 185 controls, we applied a two-phased approach of recursive partitioning and logistic regression analyses to explore complex interactions. For women only, we observed an epistatic interaction of UCHL1 and alpha-synuclein genotypes with significant effects on PD risk (odds ratio = 2.42; P = 0.003). Our findings are consistent with the hypothesis that PD is a multigenic disorder of the UPS.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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