Serveur d'exploration sur la maladie de Parkinson

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Multiple candidate gene analysis identifies α-synuclein as a susceptibility gene for sporadic Parkinson's disease

Identifieur interne : 000514 ( Main/Curation ); précédent : 000513; suivant : 000515

Multiple candidate gene analysis identifies α-synuclein as a susceptibility gene for sporadic Parkinson's disease

Auteurs : Ikuko Mizuta ; Wataru Satake ; Yuko Nakabayashi ; Chiyomi Ito ; Satoko Suzuki ; Yoshio Momose ; Yoshitaka Nagai ; Akira Oka ; Hidetoshi Inoko ; Jiro Fukae ; Yuko Saito ; Motoji Sawabe ; Shigeo Murayama ; Mitsutoshi Yamamoto ; Nobutaka Hattori ; Miho Murata [Japon] ; Tatsushi Toda [Japon]

Source :

RBID : ISTEX:D66103F44B7C0A027672E53C0AC8CA54EFD09265

Abstract

Parkinson's disease (PD), one of the most common human neurodegenerative diseases, is characterized by the loss of dopaminergic neurons in the substantia nigra of the midbrain. PD is a complex disorder with multiple genetic and environmental factors influencing disease risk. To identify susceptible genes for sporadic PD, we performed case–control association studies of 268 single nucleotide polymorphisms (SNPs) in 121 candidate genes. In two independent case–control populations, we found that a SNP in α-synuclein (SNCA), rs7684318, showed the strongest association with PD (P=5.0×10−10). Linkage disequilibrium (LD) analysis using 29 SNPs in a region around rs7684318 revealed that the entire SNCA gene lies within a single LD block (D′>0.9) spanning ∼120 kb. A tight LD group (r2>0.85) of six SNPs, including rs7684318, associated most strongly with PD (P=2.0×10−9–1.7×10−11). Haplotype association analysis did not show lower P-values than any single SNP within this group. SNCA is a major component of Lewy bodies, the pathological hallmark of PD. Aggregation of SNCA is thought to play a crucial role in PD. SNCA expression levels tended to be positively correlated with the number of the associated allele in autopsied frontal cortices. These findings establish SNCA as a definite susceptibility gene for sporadic PD.

Url:
DOI: 10.1093/hmg/ddl030

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ISTEX:D66103F44B7C0A027672E53C0AC8CA54EFD09265

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Ikuko Mizuta
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Wataru Satake
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Yuko Nakabayashi
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Yuko Nakabayashi
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Chiyomi Ito
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Chiyomi Ito
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Satoko Suzuki
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Satoko Suzuki
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Yoshio Momose
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Yoshitaka Nagai
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Akira Oka
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Hidetoshi Inoko
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Jiro Fukae
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Yuko Saito
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Yuko Saito
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Motoji Sawabe
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Shigeo Murayama
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Mitsutoshi Yamamoto
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Nobutaka Hattori
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Tatsushi Toda
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Tatsushi Toda
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<name sortKey="Sawabe, Motoji" sort="Sawabe, Motoji" uniqKey="Sawabe M" first="Motoji" last="Sawabe">Motoji Sawabe</name>
<affiliation>
<mods:affiliation>Department of Pathology, Tokyo Metropolitan Geriatric Hospital, Tokyo 173-0015, Japan,</mods:affiliation>
<wicri:noCountry code="subField"></wicri:noCountry>
</affiliation>
</author>
<author>
<name sortKey="Murayama, Shigeo" sort="Murayama, Shigeo" uniqKey="Murayama S" first="Shigeo" last="Murayama">Shigeo Murayama</name>
<affiliation>
<mods:affiliation>Department of Neuropathology, Tokyo Metropolitan Institute of Gerontology, Tokyo 173-0015, Japan,</mods:affiliation>
<wicri:noCountry code="subField"></wicri:noCountry>
</affiliation>
</author>
<author>
<name sortKey="Yamamoto, Mitsutoshi" sort="Yamamoto, Mitsutoshi" uniqKey="Yamamoto M" first="Mitsutoshi" last="Yamamoto">Mitsutoshi Yamamoto</name>
<affiliation>
<mods:affiliation>Department of Neurology, Kagawa Prefectural Central Hospital, Takamatsu 760-8557, Japan and</mods:affiliation>
<wicri:noCountry code="subField">Japan and</wicri:noCountry>
</affiliation>
</author>
<author>
<name sortKey="Hattori, Nobutaka" sort="Hattori, Nobutaka" uniqKey="Hattori N" first="Nobutaka" last="Hattori">Nobutaka Hattori</name>
<affiliation>
<mods:affiliation>Department of Neurology, Juntendo University School of Medicine, Tokyo 113-8421, Japan,</mods:affiliation>
<wicri:noCountry code="subField"></wicri:noCountry>
</affiliation>
</author>
<author>
<name sortKey="Murata, Miho" sort="Murata, Miho" uniqKey="Murata M" first="Miho" last="Murata">Miho Murata</name>
<affiliation wicri:level="1">
<mods:affiliation>Department of Neurology, Musashi Hospital, National Center of Neurology and Psychiatry, Tokyo 187-8551, Japan</mods:affiliation>
<country xml:lang="fr">Japon</country>
<wicri:regionArea>Department of Neurology, Musashi Hospital, National Center of Neurology and Psychiatry, Tokyo 187-8551</wicri:regionArea>
</affiliation>
</author>
<author>
<name sortKey="Toda, Tatsushi" sort="Toda, Tatsushi" uniqKey="Toda T" first="Tatsushi" last="Toda">Tatsushi Toda</name>
<affiliation>
<mods:affiliation>Division of Clinical Genetics, Department of Medical Genetics, Osaka University Graduate School of Medicine, 2-2-B9 Yamadaoka, Suita, Osaka 565-0871, Japan,</mods:affiliation>
<wicri:noCountry code="subField"></wicri:noCountry>
</affiliation>
<affiliation>
<mods:affiliation>Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency, Saitama 332-0012, Japan,</mods:affiliation>
<wicri:noCountry code="subField"></wicri:noCountry>
</affiliation>
<affiliation wicri:level="1">
<mods:affiliation>E-mail: toda@clgene.med.osaka-u.ac.jp</mods:affiliation>
<country wicri:rule="url">Japon</country>
</affiliation>
</author>
</analytic>
<monogr></monogr>
<series>
<title level="j">Human Molecular Genetics</title>
<title level="j" type="abbrev">Hum. Mol. Genet.</title>
<idno type="ISSN">0964-6906</idno>
<idno type="eISSN">1460-2083</idno>
<imprint>
<publisher>Oxford University Press</publisher>
<date type="published" when="2006-04-01">2006-04-01</date>
<biblScope unit="volume">15</biblScope>
<biblScope unit="issue">7</biblScope>
<biblScope unit="page" from="1151">1151</biblScope>
<biblScope unit="page" to="1158">1158</biblScope>
</imprint>
<idno type="ISSN">0964-6906</idno>
</series>
<idno type="istex">D66103F44B7C0A027672E53C0AC8CA54EFD09265</idno>
<idno type="DOI">10.1093/hmg/ddl030</idno>
<idno type="href">ddl030</idno>
<idno type="local">ddl030</idno>
</biblStruct>
</sourceDesc>
<seriesStmt>
<idno type="ISSN">0964-6906</idno>
</seriesStmt>
</fileDesc>
<profileDesc>
<textClass></textClass>
<langUsage>
<language ident="en">en</language>
</langUsage>
</profileDesc>
</teiHeader>
<front>
<div type="abstract" xml:lang="en">Parkinson's disease (PD), one of the most common human neurodegenerative diseases, is characterized by the loss of dopaminergic neurons in the substantia nigra of the midbrain. PD is a complex disorder with multiple genetic and environmental factors influencing disease risk. To identify susceptible genes for sporadic PD, we performed case–control association studies of 268 single nucleotide polymorphisms (SNPs) in 121 candidate genes. In two independent case–control populations, we found that a SNP in α-synuclein (SNCA), rs7684318, showed the strongest association with PD (P=5.0×10−10). Linkage disequilibrium (LD) analysis using 29 SNPs in a region around rs7684318 revealed that the entire SNCA gene lies within a single LD block (D′>0.9) spanning ∼120 kb. A tight LD group (r2>0.85) of six SNPs, including rs7684318, associated most strongly with PD (P=2.0×10−9–1.7×10−11). Haplotype association analysis did not show lower P-values than any single SNP within this group. SNCA is a major component of Lewy bodies, the pathological hallmark of PD. Aggregation of SNCA is thought to play a crucial role in PD. SNCA expression levels tended to be positively correlated with the number of the associated allele in autopsied frontal cortices. These findings establish SNCA as a definite susceptibility gene for sporadic PD.</div>
</front>
</TEI>
</record>

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