Somatic Alpha-Synuclein Mutations in Parkinson's Disease: Hypothesis and Preliminary Data
Identifieur interne : 000776 ( Main/Exploration ); précédent : 000775; suivant : 000777Somatic Alpha-Synuclein Mutations in Parkinson's Disease: Hypothesis and Preliminary Data
Auteurs : Christos Proukakis [Royaume-Uni] ; Henry Houlden [Royaume-Uni] ; Anthony H. Schapira [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 2013.
English descriptors
- KwdEn :
- MESH :
- chemical , genetics : alpha-Synuclein.
- genetics : Mutation, Parkinson Disease.
- Animals, Genetic Predisposition to Disease, Humans.
Abstract
Alpha-synuclein (SNCA) is crucial in the pathogenesis of Parkinson's disease (PD), yet mutations in the
Url:
DOI: 10.1002/mds.25502
PubMed: 23674490
PubMed Central: 3739940
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Somatic Alpha-Synuclein Mutations in Parkinson's Disease: Hypothesis and Preliminary Data</title><author><name sortKey="Proukakis, Christos" sort="Proukakis, Christos" uniqKey="Proukakis C" first="Christos" last="Proukakis">Christos Proukakis</name><affiliation wicri:level="1"><nlm:aff id="au1"><institution>Department of Clinical Neuroscience, Institute of Neurology, University College London</institution><addr-line>London, United Kingdom</addr-line></nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>London</wicri:regionArea></affiliation></author><author><name sortKey="Houlden, Henry" sort="Houlden, Henry" uniqKey="Houlden H" first="Henry" last="Houlden">Henry Houlden</name><affiliation wicri:level="1"><nlm:aff id="au2"><institution>Department of Molecular Neuroscience, Institute of Neurology, University College London</institution><addr-line>London, United Kingdom</addr-line></nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>London</wicri:regionArea></affiliation></author><author><name sortKey="Schapira, Anthony H" sort="Schapira, Anthony H" uniqKey="Schapira A" first="Anthony H" last="Schapira">Anthony H. Schapira</name><affiliation wicri:level="1"><nlm:aff id="au1"><institution>Department of Clinical Neuroscience, Institute of Neurology, University College London</institution><addr-line>London, United Kingdom</addr-line></nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>London</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">23674490</idno><idno type="pmc">3739940</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3739940</idno><idno type="RBID">PMC:3739940</idno><idno type="doi">10.1002/mds.25502</idno><date when="2013">2013</date><idno type="wicri:Area/Pmc/Corpus">000450</idno><idno type="wicri:Area/Pmc/Curation">000450</idno><idno type="wicri:Area/Pmc/Checkpoint">000069</idno><idno type="wicri:source">PubMed</idno><idno type="wicri:Area/PubMed/Corpus">000911</idno><idno type="wicri:Area/PubMed/Curation">000911</idno><idno type="wicri:Area/PubMed/Checkpoint">000795</idno><idno type="wicri:Area/Ncbi/Merge">003B70</idno><idno type="wicri:Area/Ncbi/Curation">003B70</idno><idno type="wicri:Area/Ncbi/Checkpoint">003B70</idno><idno type="wicri:doubleKey">0885-3185:2013:Proukakis C:somatic:alpha:synuclein</idno><idno type="wicri:Area/Main/Merge">000776</idno><idno type="wicri:Area/Main/Curation">000776</idno><idno type="wicri:Area/Main/Exploration">000776</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Somatic Alpha-Synuclein Mutations in Parkinson's Disease: Hypothesis and Preliminary Data</title><author><name sortKey="Proukakis, Christos" sort="Proukakis, Christos" uniqKey="Proukakis C" first="Christos" last="Proukakis">Christos Proukakis</name><affiliation wicri:level="1"><nlm:aff id="au1"><institution>Department of Clinical Neuroscience, Institute of Neurology, University College London</institution><addr-line>London, United Kingdom</addr-line></nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>London</wicri:regionArea></affiliation></author><author><name sortKey="Houlden, Henry" sort="Houlden, Henry" uniqKey="Houlden H" first="Henry" last="Houlden">Henry Houlden</name><affiliation wicri:level="1"><nlm:aff id="au2"><institution>Department of Molecular Neuroscience, Institute of Neurology, University College London</institution><addr-line>London, United Kingdom</addr-line></nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>London</wicri:regionArea></affiliation></author><author><name sortKey="Schapira, Anthony H" sort="Schapira, Anthony H" uniqKey="Schapira A" first="Anthony H" last="Schapira">Anthony H. Schapira</name><affiliation wicri:level="1"><nlm:aff id="au1"><institution>Department of Clinical Neuroscience, Institute of Neurology, University College London</institution><addr-line>London, United Kingdom</addr-line></nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>London</wicri:regionArea></affiliation></author></analytic><series><title level="j">Movement Disorders</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><date when="2013">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Genetic Predisposition to Disease</term><term>Humans</term><term>Mutation (genetics)</term><term>Parkinson Disease (genetics)</term><term>alpha-Synuclein (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Mutation</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Genetic Predisposition to Disease</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Alpha-synuclein (SNCA) is crucial in the pathogenesis of Parkinson's disease (PD), yet mutations in the <italic>SNCA</italic> gene are rare. Evidence for somatic genetic variation in normal humans, also involving the brain, is increasing, but its role in disease is unknown. Somatic <italic>SNCA</italic> mutations, arising in early development and leading to mosaicism, could contribute to PD pathogenesis and yet be absent or undetectable in DNA derived from peripheral lymphocytes. Such mutations could underlie the widespread pathology in PD, with the precise clinical outcome dependent on their type and the timing and location of their occurrence. We recently reported a novel <italic>SNCA</italic> mutation (c.150T>G, p.H50Q) in PD brain-derived DNA. To determine if there was mosaicism for this, a PCR and cloning strategy was used to take advantage of a nearby heterozygous intronic polymorphism. No evidence of mosaicism was found. High-resolution melting curve analysis of <italic>SNCA</italic> coding exons, which was shown to be sensitive enough to detect low proportions of 2 known mutations, did not reveal any further mutations in DNA from 28 PD brain-derived samples. We outline the grounds that make the somatic <italic>SNCA</italic> mutation hypothesis consistent with genetic, embryological, and pathological data. 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last="Proukakis">Christos Proukakis</name></noRegion><name sortKey="Houlden, Henry" sort="Houlden, Henry" uniqKey="Houlden H" first="Henry" last="Houlden">Henry Houlden</name><name sortKey="Schapira, Anthony H" sort="Schapira, Anthony H" uniqKey="Schapira A" first="Anthony H" last="Schapira">Anthony H. 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