Does α-Synuclein Have A Dual and Opposing Effect in Preclinical versus Clinical Parkinson’s Disease?
Identifieur interne : 000899 ( Pmc/Curation ); précédent : 000898; suivant : 000900Does α-Synuclein Have A Dual and Opposing Effect in Preclinical versus Clinical Parkinson’s Disease?
Auteurs : Katerina Markopoulou [États-Unis] ; Joanna M. Biernacka [États-Unis] ; Sebastian M. Armasu [États-Unis] ; Kari J. Anderson [États-Unis] ; J. Eric Ahlskog [États-Unis] ; Bruce A. Chase [États-Unis] ; Sun Ju Chung [Corée du Sud] ; Julie M. Cunningham [États-Unis] ; Matthew Farrer [Canada] ; Roberta Frigerio [États-Unis] ; Demetrius M. Maraganore [États-Unis]Source :
- Parkinsonism & related disorders [ 1353-8020 ] ; 2014.
Abstract
α-Synuclein gene (
Url:
DOI: 10.1016/j.parkreldis.2014.02.021
PubMed: 24656894
PubMed Central: 4723426
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<author><name sortKey="Chung, Sun Ju" sort="Chung, Sun Ju" uniqKey="Chung S" first="Sun Ju" last="Chung">Sun Ju Chung</name>
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</placeName>
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<series><title level="j">Parkinsonism & related disorders</title>
<idno type="ISSN">1353-8020</idno>
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<front><div type="abstract" xml:lang="en"><p id="P2">α-Synuclein gene (<italic>SNCA</italic>
) multiplications cause familial parkinsonism and allele-length polymorphisms within the <italic>SNCA</italic>
dinucleotide repeat REP1 increase the risk for developing Parkinson’s disease (PD). Since <italic>SNCA</italic>
multiplications increase <italic>SNCA</italic>
expression, and REP1-genotypes that increase the risk of developing PD show increased <italic>SNCA</italic>
expression in cell-culture systems, animal models, and human blood and brain, PD therapies seek to reduce <italic>SNCA</italic>
expression. We conducted an observational study of 1,098 PD cases to test the hypothesis that REP1 genotypes correlated with reduced <italic>SNCA</italic>
expression are associated with better motor and cognitive outcomes. We evaluated the association of REP1 genotypes with survival free of Hoehn and Yahr stages 4 or 5 (motor outcome) and of Modified Telephone Interview for Cognitive Status score ≤27 or Alzheimer’s Disease-8 score ≥2 (cognitive outcome). Median disease duration at baseline was 3.3 years and median lag time from baseline to follow-up was 7.8 years. Paradoxically, REP1 genotypes associated with increased risk of developing PD and increased <italic>SNCA</italic>
expression were associated with better motor (HR=0.87, p=0.046 covariate-adjusted age-scale analysis; HR=0.85, p=0.020, covariate-adjusted time-scale analysis) and cognitive outcomes (HR=0.90, p=0.12, covariate-adjusted age-scale analysis; HR=0.85, p=0.023, covariate-adjusted time-scale analysis). Our findings raise the possibility that <italic>SNCA</italic>
has a dual, opposing, and time-dependent role. This may have implications for the development of therapies that target <italic>SNCA</italic>
expression.</p>
</div>
</front>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">9513583</journal-id>
<journal-id journal-id-type="pubmed-jr-id">21522</journal-id>
<journal-id journal-id-type="nlm-ta">Parkinsonism Relat Disord</journal-id>
<journal-id journal-id-type="iso-abbrev">Parkinsonism Relat. Disord.</journal-id>
<journal-title-group><journal-title>Parkinsonism & related disorders</journal-title>
</journal-title-group>
<issn pub-type="ppub">1353-8020</issn>
<issn pub-type="epub">1873-5126</issn>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">24656894</article-id>
<article-id pub-id-type="pmc">4723426</article-id>
<article-id pub-id-type="doi">10.1016/j.parkreldis.2014.02.021</article-id>
<article-id pub-id-type="manuscript">NIHMS572902</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Does α-Synuclein Have A Dual and Opposing Effect in Preclinical versus Clinical Parkinson’s Disease?</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Markopoulou</surname>
<given-names>Katerina</given-names>
</name>
<degrees>MD, PhD</degrees>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Biernacka</surname>
<given-names>Joanna M.</given-names>
</name>
<degrees>PhD</degrees>
<xref ref-type="aff" rid="A2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Armasu</surname>
<given-names>Sebastian M.</given-names>
</name>
<degrees>MS</degrees>
<xref ref-type="aff" rid="A2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Anderson</surname>
<given-names>Kari J.</given-names>
</name>
<degrees>BS</degrees>
<xref ref-type="aff" rid="A2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Ahlskog</surname>
<given-names>J. Eric</given-names>
</name>
<degrees>PhD, MD</degrees>
<xref ref-type="aff" rid="A3">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Chase</surname>
<given-names>Bruce A.</given-names>
</name>
<degrees>PhD</degrees>
<xref ref-type="aff" rid="A4">4</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Chung</surname>
<given-names>Sun Ju</given-names>
</name>
<degrees>MD</degrees>
<xref ref-type="aff" rid="A5">5</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Cunningham</surname>
<given-names>Julie M.</given-names>
</name>
<degrees>PhD</degrees>
<xref ref-type="aff" rid="A6">6</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Farrer</surname>
<given-names>Matthew</given-names>
</name>
<degrees>PhD</degrees>
<xref ref-type="aff" rid="A7">7</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Frigerio</surname>
<given-names>Roberta</given-names>
</name>
<degrees>MD</degrees>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Maraganore</surname>
<given-names>Demetrius M.</given-names>
</name>
<degrees>MD</degrees>
<xref ref-type="aff" rid="A1">1</xref>
<xref rid="FN1" ref-type="author-notes">*</xref>
</contrib>
</contrib-group>
<aff id="A1"><label>1</label>
Department of Neurology, NorthShore University HealthSystem, Evanston, IL USA</aff>
<aff id="A2"><label>2</label>
Department of Health Sciences Research, Mayo Clinic, Rochester, MN USA</aff>
<aff id="A3"><label>3</label>
Department of Neurology, Mayo Clinic, Rochester, MN USA</aff>
<aff id="A4"><label>4</label>
Department of Biology, University of Nebraska at Omaha, Omaha, NE USA</aff>
<aff id="A5"><label>5</label>
Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea</aff>
<aff id="A6"><label>6</label>
Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN USA</aff>
<aff id="A7"><label>7</label>
Centre for Applied Neurogenetics, University of British Columbia, Vancouver, BC, Canada</aff>
<author-notes><corresp id="FN1"><label>*</label>
Corresponding Author: Dr. Demetrius M. Maraganore, Ruth Cain Ruggles Chairman, Department of Neurology, NorthShore University Health System, 2650 Ridge Avenue, Evanston, IL 60201., <email>dmaraganore@northshore.org</email>
, Telephone: +1 847 570 1678, Fax: +1 847 733 5565</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>23</day>
<month>12</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="epub"><day>05</day>
<month>3</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="ppub"><month>6</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>23</day>
<month>1</month>
<year>2016</year>
</pub-date>
<volume>20</volume>
<issue>6</issue>
<fpage>584</fpage>
<lpage>584</lpage>
<pmc-comment>elocation-id from pubmed: 10.1016/j.parkreldis.2014.02.021</pmc-comment>
<abstract><p id="P2">α-Synuclein gene (<italic>SNCA</italic>
) multiplications cause familial parkinsonism and allele-length polymorphisms within the <italic>SNCA</italic>
dinucleotide repeat REP1 increase the risk for developing Parkinson’s disease (PD). Since <italic>SNCA</italic>
multiplications increase <italic>SNCA</italic>
expression, and REP1-genotypes that increase the risk of developing PD show increased <italic>SNCA</italic>
expression in cell-culture systems, animal models, and human blood and brain, PD therapies seek to reduce <italic>SNCA</italic>
expression. We conducted an observational study of 1,098 PD cases to test the hypothesis that REP1 genotypes correlated with reduced <italic>SNCA</italic>
expression are associated with better motor and cognitive outcomes. We evaluated the association of REP1 genotypes with survival free of Hoehn and Yahr stages 4 or 5 (motor outcome) and of Modified Telephone Interview for Cognitive Status score ≤27 or Alzheimer’s Disease-8 score ≥2 (cognitive outcome). Median disease duration at baseline was 3.3 years and median lag time from baseline to follow-up was 7.8 years. Paradoxically, REP1 genotypes associated with increased risk of developing PD and increased <italic>SNCA</italic>
expression were associated with better motor (HR=0.87, p=0.046 covariate-adjusted age-scale analysis; HR=0.85, p=0.020, covariate-adjusted time-scale analysis) and cognitive outcomes (HR=0.90, p=0.12, covariate-adjusted age-scale analysis; HR=0.85, p=0.023, covariate-adjusted time-scale analysis). Our findings raise the possibility that <italic>SNCA</italic>
has a dual, opposing, and time-dependent role. This may have implications for the development of therapies that target <italic>SNCA</italic>
expression.</p>
</abstract>
<kwd-group><kwd>Parkinson’s disease</kwd>
<kwd>α-synuclein gene</kwd>
<kwd>outcomes</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>
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