Genomewide association study for onset age in Parkinson disease.
Identifieur interne : 000107 ( PubMed/Curation ); précédent : 000106; suivant : 000108Genomewide association study for onset age in Parkinson disease.
Auteurs : Jeanne. Latourelle [États-Unis] ; Nathan Pankratz ; Alexandra Dumitriu ; Jemma. Wilk ; Stefano Goldwurm ; Gianni Pezzoli ; Claudio. Mariani ; Anita. Destefano ; Cheryl Halter ; James. Gusella ; William. Nichols ; Richard. Myers ; Tatiana ForoudSource :
- BMC medical genetics ; 2009.
English descriptors
- KwdEn :
- MESH :
Abstract
Age at onset in Parkinson disease (PD) is a highly heritable quantitative trait for which a significant genetic influence is supported by multiple segregation analyses. Because genes associated with onset age may represent invaluable therapeutic targets to delay the disease, we sought to identify such genetic modifiers using a genomewide association study in familial PD. There have been previous genomewide association studies (GWAS) to identify genes influencing PD susceptibility, but this is the first to identify genes contributing to the variation in onset age.
DOI: 10.1186/1471-2350-10-98
PubMed: 19772629
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<author><name sortKey="Destefano, Anita L" sort="Destefano, Anita L" uniqKey="Destefano A" first="Anita" last="Destefano">Anita. Destefano</name>
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<author><name sortKey="Halter, Cheryl" sort="Halter, Cheryl" uniqKey="Halter C" first="Cheryl" last="Halter">Cheryl Halter</name>
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<author><name sortKey="Gusella, James F" sort="Gusella, James F" uniqKey="Gusella J" first="James" last="Gusella">James. Gusella</name>
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<author><name sortKey="Nichols, William C" sort="Nichols, William C" uniqKey="Nichols W" first="William" last="Nichols">William. Nichols</name>
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<author><name sortKey="Myers, Richard H" sort="Myers, Richard H" uniqKey="Myers R" first="Richard" last="Myers">Richard. Myers</name>
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<author><name sortKey="Foroud, Tatiana" sort="Foroud, Tatiana" uniqKey="Foroud T" first="Tatiana" last="Foroud">Tatiana Foroud</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term>
<term>Age of Onset</term>
<term>Aged</term>
<term>Aged, 80 and over</term>
<term>Female</term>
<term>Genome-Wide Association Study</term>
<term>Humans</term>
<term>Linear Models</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Parkinson Disease (genetics)</term>
<term>Polymorphism, Single Nucleotide</term>
<term>Young Adult</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Adult</term>
<term>Age of Onset</term>
<term>Aged</term>
<term>Aged, 80 and over</term>
<term>Female</term>
<term>Genome-Wide Association Study</term>
<term>Humans</term>
<term>Linear Models</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Polymorphism, Single Nucleotide</term>
<term>Young Adult</term>
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<front><div type="abstract" xml:lang="en">Age at onset in Parkinson disease (PD) is a highly heritable quantitative trait for which a significant genetic influence is supported by multiple segregation analyses. Because genes associated with onset age may represent invaluable therapeutic targets to delay the disease, we sought to identify such genetic modifiers using a genomewide association study in familial PD. There have been previous genomewide association studies (GWAS) to identify genes influencing PD susceptibility, but this is the first to identify genes contributing to the variation in onset age.</div>
</front>
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<pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">19772629</PMID>
<DateCreated><Year>2009</Year>
<Month>10</Month>
<Day>07</Day>
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<DateCompleted><Year>2009</Year>
<Month>10</Month>
<Day>07</Day>
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<DateRevised><Year>2014</Year>
<Month>12</Month>
<Day>07</Day>
</DateRevised>
<Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1471-2350</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>10</Volume>
<PubDate><Year>2009</Year>
</PubDate>
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<Title>BMC medical genetics</Title>
<ISOAbbreviation>BMC Med. Genet.</ISOAbbreviation>
</Journal>
<ArticleTitle>Genomewide association study for onset age in Parkinson disease.</ArticleTitle>
<Pagination><MedlinePgn>98</MedlinePgn>
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<ELocationID EIdType="doi" ValidYN="Y">10.1186/1471-2350-10-98</ELocationID>
<Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Age at onset in Parkinson disease (PD) is a highly heritable quantitative trait for which a significant genetic influence is supported by multiple segregation analyses. Because genes associated with onset age may represent invaluable therapeutic targets to delay the disease, we sought to identify such genetic modifiers using a genomewide association study in familial PD. There have been previous genomewide association studies (GWAS) to identify genes influencing PD susceptibility, but this is the first to identify genes contributing to the variation in onset age.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">Initial analyses were performed using genotypes generated with the Illumina HumanCNV370Duo array in a sample of 857 unrelated, familial PD cases. Subsequently, a meta-analysis of imputed SNPs was performed combining the familial PD data with that from a previous GWAS of 440 idiopathic PD cases. The SNPs from the meta-analysis with the lowest p-values and consistency in the direction of effect for onset age were then genotyped in a replication sample of 747 idiopathic PD cases from the Parkinson Institute Biobank of Milan, Italy.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">Meta-analysis across the three studies detected consistent association (p < 1 x 10(-5)) with five SNPs, none of which reached genomewide significance. On chromosome 11, the SNP with the lowest p-value (rs10767971; p = 5.4 x 10(-7)) lies between the genes QSER1 and PRRG4. Near the PARK3 linkage region on chromosome 2p13, association was observed with a SNP (rs7577851; p = 8.7 x 10(-6)) which lies in an intron of the AAK1 gene. This gene is closely related to GAK, identified as a possible PD susceptibility gene in the GWAS of the familial PD cases.</AbstractText>
<AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Taken together, these results suggest an influence of genes involved in endocytosis and lysosomal sorting in PD pathogenesis.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Latourelle</LastName>
<ForeName>Jeanne C</ForeName>
<Initials>JC</Initials>
<AffiliationInfo><Affiliation>Boston University School of Medicine, Boston, MA, USA. jlatoure@bu.edu</Affiliation>
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<Author ValidYN="Y"><LastName>Dumitriu</LastName>
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<Author ValidYN="Y"><CollectiveName>PROGENI Investigators, Coordinators and Molecular Genetic Laboratories</CollectiveName>
</Author>
<Author ValidYN="Y"><CollectiveName>GenePD Investigators, Coordinators and Molecular Genetic Laboratories</CollectiveName>
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