Cerebrospinal Fluid α-Synuclein Predicts Cognitive Decline in Parkinson Disease Progression in the DATATOP Cohort
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Auteurs : Tessandra Stewart [États-Unis] ; Changqin Liu [États-Unis, République populaire de Chine] ; Carmen Ginghina [États-Unis] ; Kevin Cain [États-Unis] ; Peggy Auinger [États-Unis] ; Brenna Cholerton [États-Unis] ; Min Shi [États-Unis] ; Jing Zhang [États-Unis]Source :
- The American Journal of Pathology [ 0002-9440 ] ; 2014.
Abstract
Most patients with Parkinson disease (PD) develop both cognitive and motor impairment, and biomarkers for progression are urgently needed. Although α-synuclein is altered in cerebrospinal fluid of patients with PD, it is not known whether it predicts motor or cognitive deterioration. We examined clinical data and α-synuclein in >300 unmedicated patients with PD who participated in the deprenyl and tocopherol antioxidative therapy of parkinsonism (DATATOP) study, with up to 8 years of follow-up. Longitudinal measures of motor and cognitive function were studied before (phase 1) and during (phase 2) levodopa therapy; cerebrospinal fluid was collected at the beginning of each phase. Correlations and linear mixed models were used to assess α-synuclein association with disease severity and prediction of progression in the subsequent follow-up period. Despite decreasing α-synuclein (phase 1 to phase 2 change of −0.05 ± 0.21 log-transformed values,
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DOI: 10.1016/j.ajpath.2013.12.007
PubMed: 24625392
PubMed Central: 3969999
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type="wicri:Area/Pmc/Curation">000221</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Cerebrospinal Fluid α-Synuclein Predicts Cognitive Decline in Parkinson Disease Progression in the DATATOP Cohort</title><author><name sortKey="Stewart, Tessandra" sort="Stewart, Tessandra" uniqKey="Stewart T" first="Tessandra" last="Stewart">Tessandra Stewart</name><affiliation wicri:level="2"><nlm:aff id="aff1">Department of Pathology, University of Washington School of Medicine, Seattle, Washington</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Washington (État)</region></placeName><wicri:cityArea>Department of Pathology, University of Washington School of Medicine, Seattle</wicri:cityArea></affiliation></author><author><name sortKey="Liu, Changqin" sort="Liu, Changqin" uniqKey="Liu C" first="Changqin" last="Liu">Changqin Liu</name><affiliation wicri:level="2"><nlm:aff id="aff1">Department of Pathology, University of Washington School of Medicine, Seattle, Washington</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Washington (État)</region></placeName><wicri:cityArea>Department of Pathology, University of Washington School of Medicine, Seattle</wicri:cityArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff3">Department of Endocrinology and Metabolism and Xiamen Diabetes Institute, the First Affiliated Hospital of Xiamen University, Xiamen, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Endocrinology and Metabolism and Xiamen Diabetes Institute, the First Affiliated Hospital of Xiamen University, Xiamen</wicri:regionArea></affiliation></author><author><name sortKey="Ginghina, Carmen" sort="Ginghina, Carmen" uniqKey="Ginghina C" first="Carmen" last="Ginghina">Carmen Ginghina</name><affiliation wicri:level="2"><nlm:aff id="aff1">Department of Pathology, University of Washington School of Medicine, Seattle, Washington</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Washington (État)</region></placeName><wicri:cityArea>Department of Pathology, University of Washington School of Medicine, Seattle</wicri:cityArea></affiliation></author><author><name sortKey="Cain, Kevin C" sort="Cain, Kevin C" uniqKey="Cain K" first="Kevin" last="Cain">Kevin Cain</name><affiliation wicri:level="2"><nlm:aff id="aff4">Department of Biostatistics, University of Washington School of Public Health, Seattle, Washington</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Washington (État)</region></placeName><wicri:cityArea>Department of Biostatistics, University of Washington School of Public Health, Seattle</wicri:cityArea></affiliation></author><author><name sortKey="Auinger, Peggy" sort="Auinger, Peggy" uniqKey="Auinger P" first="Peggy" last="Auinger">Peggy Auinger</name><affiliation wicri:level="2"><nlm:aff id="aff5">Department of Neurology, the Center for Human Experimental Therapeutics, University of Rochester School of Medicine and Dentistry, Rochester, New York</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">État de New York</region></placeName><wicri:cityArea>Department of Neurology, the Center for Human Experimental Therapeutics, University of Rochester School of Medicine and Dentistry, Rochester</wicri:cityArea></affiliation></author><author><name sortKey="Cholerton, Brenna" sort="Cholerton, Brenna" uniqKey="Cholerton B" first="Brenna" last="Cholerton">Brenna Cholerton</name><affiliation wicri:level="2"><nlm:aff id="aff2">Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, Washington</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Washington (État)</region></placeName><wicri:cityArea>Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:aff id="aff6">Geriatric Research, Education, and Clinical Center, Veterans Affairs of Puget Sound Health Care System, Seattle, Washington</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Washington (État)</region></placeName><wicri:cityArea>Geriatric Research, Education, and Clinical Center, Veterans Affairs of Puget Sound Health Care System, Seattle</wicri:cityArea></affiliation></author><author><name sortKey="Shi, Min" sort="Shi, Min" uniqKey="Shi M" first="Min" last="Shi">Min Shi</name><affiliation wicri:level="2"><nlm:aff id="aff1">Department of Pathology, University of Washington School of Medicine, Seattle, Washington</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Washington (État)</region></placeName><wicri:cityArea>Department of Pathology, University of Washington School of Medicine, Seattle</wicri:cityArea></affiliation></author><author><name sortKey="Zhang, Jing" sort="Zhang, Jing" uniqKey="Zhang J" first="Jing" last="Zhang">Jing Zhang</name><affiliation wicri:level="2"><nlm:aff id="aff1">Department of Pathology, University of Washington School of Medicine, Seattle, Washington</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Washington (État)</region></placeName><wicri:cityArea>Department of Pathology, University of Washington School of Medicine, Seattle</wicri:cityArea></affiliation></author></analytic><series><title level="j">The American Journal of Pathology</title><idno type="ISSN">0002-9440</idno><idno type="e-ISSN">1525-2191</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Most patients with Parkinson disease (PD) develop both cognitive and motor impairment, and biomarkers for progression are urgently needed. Although α-synuclein is altered in cerebrospinal fluid of patients with PD, it is not known whether it predicts motor or cognitive deterioration. We examined clinical data and α-synuclein in >300 unmedicated patients with PD who participated in the deprenyl and tocopherol antioxidative therapy of parkinsonism (DATATOP) study, with up to 8 years of follow-up. Longitudinal measures of motor and cognitive function were studied before (phase 1) and during (phase 2) levodopa therapy; cerebrospinal fluid was collected at the beginning of each phase. Correlations and linear mixed models were used to assess α-synuclein association with disease severity and prediction of progression in the subsequent follow-up period. Despite decreasing α-synuclein (phase 1 to phase 2 change of −0.05 ± 0.21 log-transformed values, <italic>P</italic> < 0.001), no correlations were observed between α-synuclein and motor symptoms. Longitudinally, lower α-synuclein predicted better preservation of cognitive function by several measures [Selective Reminding Test total recall α-synuclein × time interaction effect coefficient, −0.12 (<italic>P</italic> = 0.037); delayed recall, −0.05 (<italic>P</italic> = 0.002); New Dot Test, −0.03 (<italic>P</italic> = 0.002)]. Thus, α-synuclein, although not clinically useful for motor progression, might predict cognitive decline, and future longitudinal studies should include this outcome for further validation.</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>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Am J Pathol</journal-id><journal-id journal-id-type="iso-abbrev">Am. J. Pathol</journal-id><journal-title-group><journal-title>The American Journal of Pathology</journal-title></journal-title-group><issn pub-type="ppub">0002-9440</issn><issn pub-type="epub">1525-2191</issn><publisher><publisher-name>American Society for Investigative Pathology</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">24625392</article-id><article-id pub-id-type="pmc">3969999</article-id><article-id pub-id-type="publisher-id">S0002-9440(14)00012-1</article-id><article-id pub-id-type="doi">10.1016/j.ajpath.2013.12.007</article-id><article-categories><subj-group subj-group-type="heading"><subject>Regular Article</subject><subj-group><subject>Biomarkers, Genomics, Proteomics, and Gene Regulation</subject></subj-group></subj-group></article-categories><title-group><article-title>Cerebrospinal Fluid α-Synuclein Predicts Cognitive Decline in Parkinson Disease Progression in the DATATOP Cohort</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Stewart</surname><given-names>Tessandra</given-names></name><xref rid="aff1" ref-type="aff">∗</xref></contrib><contrib contrib-type="author"><name><surname>Liu</surname><given-names>Changqin</given-names></name><xref rid="aff1" ref-type="aff">∗</xref><xref rid="aff3" ref-type="aff">†</xref></contrib><contrib contrib-type="author"><name><surname>Ginghina</surname><given-names>Carmen</given-names></name><xref rid="aff1" ref-type="aff">∗</xref></contrib><contrib contrib-type="author"><name><surname>Cain</surname><given-names>Kevin C.</given-names></name><xref rid="aff4" ref-type="aff">‡</xref></contrib><contrib contrib-type="author"><name><surname>Auinger</surname><given-names>Peggy</given-names></name><xref rid="aff5" ref-type="aff">§</xref></contrib><contrib contrib-type="author"><name><surname>Cholerton</surname><given-names>Brenna</given-names></name><xref rid="aff2" ref-type="aff">¶</xref><xref rid="aff6" ref-type="aff">‖</xref></contrib><contrib contrib-type="author"><name><surname>Shi</surname><given-names>Min</given-names></name><xref rid="aff1" ref-type="aff">∗</xref></contrib><contrib contrib-type="author"><name><surname>Zhang</surname><given-names>Jing</given-names></name><email>zhangj@uw.edu</email><xref rid="aff1" ref-type="aff">∗</xref><xref rid="cor1" ref-type="corresp">∗</xref></contrib><contrib contrib-type="author"><collab>Parkinson Study Group DATATOP Investigators</collab></contrib></contrib-group><aff id="aff1"><label>∗</label>Department of Pathology, University of Washington School of Medicine, Seattle, Washington</aff><aff id="aff2"><label>¶</label>Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, Washington</aff><aff id="aff3"><label>†</label>Department of Endocrinology and Metabolism and Xiamen Diabetes Institute, the First Affiliated Hospital of Xiamen University, Xiamen, China</aff><aff id="aff4"><label>‡</label>Department of Biostatistics, University of Washington School of Public Health, Seattle, Washington</aff><aff id="aff5"><label>§</label>Department of Neurology, the Center for Human Experimental Therapeutics, University of Rochester School of Medicine and Dentistry, Rochester, New York</aff><aff id="aff6"><label>‖</label>Geriatric Research, Education, and Clinical Center, Veterans Affairs of Puget Sound Health Care System, Seattle, Washington</aff><author-notes><corresp id="cor1"><label>∗</label>Address correspondence to Jing Zhang, M.D., Ph.D., Department of Pathology, University of Washington School of Medicine, Harborview Medical Center Box 359635, 325 9th Ave, Seattle, WA 98104. <email>zhangj@uw.edu</email></corresp></author-notes><pub-date pub-type="pmc-release"><day>1</day><month>4</month><year>2015</year></pub-date><pmc-comment> PMC Release delay is 12 months and 0 days
and was based on .</pmc-comment>
<pub-date pub-type="ppub"><month>4</month><year>2014</year></pub-date><volume>184</volume><issue>4</issue><fpage>966</fpage><lpage>975</lpage><history><date date-type="accepted"><day>12</day><month>12</month><year>2013</year></date></history><permissions><copyright-statement>© 2014 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.</copyright-statement><copyright-year>2014</copyright-year><copyright-holder>American Society for Investigative Pathology</copyright-holder><license><license-p>This document may be redistributed and reused, subject to <ext-link ext-link-type="uri" xlink:href="http://www.elsevier.com/wps/find/authorsview.authors/supplementalterms1.0">certain conditions</ext-link>.</license-p></license></permissions><abstract><p>Most patients with Parkinson disease (PD) develop both cognitive and motor impairment, and biomarkers for progression are urgently needed. Although α-synuclein is altered in cerebrospinal fluid of patients with PD, it is not known whether it predicts motor or cognitive deterioration. We examined clinical data and α-synuclein in >300 unmedicated patients with PD who participated in the deprenyl and tocopherol antioxidative therapy of parkinsonism (DATATOP) study, with up to 8 years of follow-up. Longitudinal measures of motor and cognitive function were studied before (phase 1) and during (phase 2) levodopa therapy; cerebrospinal fluid was collected at the beginning of each phase. Correlations and linear mixed models were used to assess α-synuclein association with disease severity and prediction of progression in the subsequent follow-up period. Despite decreasing α-synuclein (phase 1 to phase 2 change of −0.05 ± 0.21 log-transformed values, <italic>P</italic> < 0.001), no correlations were observed between α-synuclein and motor symptoms. Longitudinally, lower α-synuclein predicted better preservation of cognitive function by several measures [Selective Reminding Test total recall α-synuclein × time interaction effect coefficient, −0.12 (<italic>P</italic> = 0.037); delayed recall, −0.05 (<italic>P</italic> = 0.002); New Dot Test, −0.03 (<italic>P</italic> = 0.002)]. Thus, α-synuclein, although not clinically useful for motor progression, might predict cognitive decline, and future longitudinal studies should include this outcome for further validation.</p></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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