Does α-synuclein have a dual and opposing effect in preclinical vs. clinical Parkinson's disease?
Identifieur interne : 000745 ( PubMed/Corpus ); précédent : 000744; suivant : 000746Does α-synuclein have a dual and opposing effect in preclinical vs. clinical Parkinson's disease?
Auteurs : Katerina Markopoulou ; Joanna M. Biernacka ; Sebastian M. Armasu ; Kari J. Anderson ; J Eric Ahlskog ; Bruce A. Chase ; Sun Ju Chung ; Julie M. Cunningham ; Matthew Farrer ; Roberta Frigerio ; Demetrius M. MaraganoreSource :
- Parkinsonism & related disorders [ 1873-5126 ] ; 2014.
English descriptors
- KwdEn :
- Adult, Aged, Aged, 80 and over, Cognition Disorders (etiology), Dinucleotide Repeats (genetics), Disability Evaluation, Female, Genotype, Humans, Kaplan-Meier Estimate, Longitudinal Studies, Male, Middle Aged, Parkinson Disease (complications), Parkinson Disease (genetics), Parkinson Disease (mortality), Polymorphism, Single Nucleotide (genetics), Proportional Hazards Models, Severity of Illness Index, Surveys and Questionnaires, alpha-Synuclein (genetics).
- MESH :
- chemical , genetics : alpha-Synuclein.
- complications : Parkinson Disease.
- etiology : Cognition Disorders.
- genetics : Dinucleotide Repeats, Parkinson Disease, Polymorphism, Single Nucleotide.
- mortality : Parkinson Disease.
- Adult, Aged, Aged, 80 and over, Disability Evaluation, Female, Genotype, Humans, Kaplan-Meier Estimate, Longitudinal Studies, Male, Middle Aged, Proportional Hazards Models, Severity of Illness Index, Surveys and Questionnaires.
Abstract
α-Synuclein gene (SNCA) multiplications cause familial parkinsonism and allele-length polymorphisms within the SNCA dinucleotide repeat REP1 increase the risk for developing Parkinson's disease (PD). Since SNCA multiplications increase SNCA expression, and REP1 genotypes that increase the risk of developing PD show increased SNCA expression in cell-culture systems, animal models, and human blood and brain, PD therapies seek to reduce SNCA expression. We conducted an observational study of 1098 PD cases to test the hypothesis that REP1 genotypes correlated with reduced SNCA 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 Dementia Screening Interview 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 SNCA 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 SNCA has a dual, opposing, and time-dependent role. This may have implications for the development of therapies that target SNCA expression.
DOI: 10.1016/j.parkreldis.2014.02.021
PubMed: 24656894
Links to Exploration step
pubmed:24656894Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Does α-synuclein have a dual and opposing effect in preclinical vs. clinical Parkinson's disease?</title><author><name sortKey="Markopoulou, Katerina" sort="Markopoulou, Katerina" uniqKey="Markopoulou K" first="Katerina" last="Markopoulou">Katerina Markopoulou</name><affiliation><nlm:affiliation>Department of Neurology, NorthShore University HealthSystem, Evanston, IL, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Biernacka, Joanna M" sort="Biernacka, Joanna M" uniqKey="Biernacka J" first="Joanna M" last="Biernacka">Joanna M. Biernacka</name><affiliation><nlm:affiliation>Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Armasu, Sebastian M" sort="Armasu, Sebastian M" uniqKey="Armasu S" first="Sebastian M" last="Armasu">Sebastian M. Armasu</name><affiliation><nlm:affiliation>Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Anderson, Kari J" sort="Anderson, Kari J" uniqKey="Anderson K" first="Kari J" last="Anderson">Kari J. Anderson</name><affiliation><nlm:affiliation>Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Ahlskog, J Eric" sort="Ahlskog, J Eric" uniqKey="Ahlskog J" first="J Eric" last="Ahlskog">J Eric Ahlskog</name><affiliation><nlm:affiliation>Department of Neurology, Mayo Clinic, Rochester, MN, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Chase, Bruce A" sort="Chase, Bruce A" uniqKey="Chase B" first="Bruce A" last="Chase">Bruce A. Chase</name><affiliation><nlm:affiliation>Department of Biology, University of Nebraska at Omaha, Omaha, NE, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Chung, Sun Ju" sort="Chung, Sun Ju" uniqKey="Chung S" first="Sun Ju" last="Chung">Sun Ju Chung</name><affiliation><nlm:affiliation>Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.</nlm:affiliation></affiliation></author><author><name sortKey="Cunningham, Julie M" sort="Cunningham, Julie M" uniqKey="Cunningham J" first="Julie M" last="Cunningham">Julie M. Cunningham</name><affiliation><nlm:affiliation>Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Farrer, Matthew" sort="Farrer, Matthew" uniqKey="Farrer M" first="Matthew" last="Farrer">Matthew Farrer</name><affiliation><nlm:affiliation>Centre for Applied Neurogenetics, University of British Columbia, Vancouver, BC, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Frigerio, Roberta" sort="Frigerio, Roberta" uniqKey="Frigerio R" first="Roberta" last="Frigerio">Roberta Frigerio</name><affiliation><nlm:affiliation>Department of Neurology, NorthShore University HealthSystem, Evanston, IL, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Maraganore, Demetrius M" sort="Maraganore, Demetrius M" uniqKey="Maraganore D" first="Demetrius M" last="Maraganore">Demetrius M. Maraganore</name><affiliation><nlm:affiliation>Department of Neurology, NorthShore University HealthSystem, Evanston, IL, USA. 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Biernacka</name><affiliation><nlm:affiliation>Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Armasu, Sebastian M" sort="Armasu, Sebastian M" uniqKey="Armasu S" first="Sebastian M" last="Armasu">Sebastian M. Armasu</name><affiliation><nlm:affiliation>Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Anderson, Kari J" sort="Anderson, Kari J" uniqKey="Anderson K" first="Kari J" last="Anderson">Kari J. Anderson</name><affiliation><nlm:affiliation>Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Ahlskog, J Eric" sort="Ahlskog, J Eric" uniqKey="Ahlskog J" first="J Eric" last="Ahlskog">J Eric Ahlskog</name><affiliation><nlm:affiliation>Department of Neurology, Mayo Clinic, Rochester, MN, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Chase, Bruce A" sort="Chase, Bruce A" uniqKey="Chase B" first="Bruce A" last="Chase">Bruce A. Chase</name><affiliation><nlm:affiliation>Department of Biology, University of Nebraska at Omaha, Omaha, NE, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Chung, Sun Ju" sort="Chung, Sun Ju" uniqKey="Chung S" first="Sun Ju" last="Chung">Sun Ju Chung</name><affiliation><nlm:affiliation>Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.</nlm:affiliation></affiliation></author><author><name sortKey="Cunningham, Julie M" sort="Cunningham, Julie M" uniqKey="Cunningham J" first="Julie M" last="Cunningham">Julie M. Cunningham</name><affiliation><nlm:affiliation>Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Farrer, Matthew" sort="Farrer, Matthew" uniqKey="Farrer M" first="Matthew" last="Farrer">Matthew Farrer</name><affiliation><nlm:affiliation>Centre for Applied Neurogenetics, University of British Columbia, Vancouver, BC, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Frigerio, Roberta" sort="Frigerio, Roberta" uniqKey="Frigerio R" first="Roberta" last="Frigerio">Roberta Frigerio</name><affiliation><nlm:affiliation>Department of Neurology, NorthShore University HealthSystem, Evanston, IL, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Maraganore, Demetrius M" sort="Maraganore, Demetrius M" uniqKey="Maraganore D" first="Demetrius M" last="Maraganore">Demetrius M. Maraganore</name><affiliation><nlm:affiliation>Department of Neurology, NorthShore University HealthSystem, Evanston, IL, USA. Electronic address: dmaraganore@northshore.org.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Parkinsonism & related disorders</title><idno type="eISSN">1873-5126</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Cognition Disorders (etiology)</term><term>Dinucleotide Repeats (genetics)</term><term>Disability Evaluation</term><term>Female</term><term>Genotype</term><term>Humans</term><term>Kaplan-Meier Estimate</term><term>Longitudinal Studies</term><term>Male</term><term>Middle Aged</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (mortality)</term><term>Polymorphism, Single Nucleotide (genetics)</term><term>Proportional Hazards Models</term><term>Severity of Illness Index</term><term>Surveys and Questionnaires</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="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Cognition Disorders</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Dinucleotide Repeats</term><term>Parkinson Disease</term><term>Polymorphism, Single Nucleotide</term></keywords><keywords scheme="MESH" qualifier="mortality" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Disability Evaluation</term><term>Female</term><term>Genotype</term><term>Humans</term><term>Kaplan-Meier Estimate</term><term>Longitudinal Studies</term><term>Male</term><term>Middle Aged</term><term>Proportional Hazards Models</term><term>Severity of Illness Index</term><term>Surveys and Questionnaires</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">α-Synuclein gene (SNCA) multiplications cause familial parkinsonism and allele-length polymorphisms within the SNCA dinucleotide repeat REP1 increase the risk for developing Parkinson's disease (PD). Since SNCA multiplications increase SNCA expression, and REP1 genotypes that increase the risk of developing PD show increased SNCA expression in cell-culture systems, animal models, and human blood and brain, PD therapies seek to reduce SNCA expression. We conducted an observational study of 1098 PD cases to test the hypothesis that REP1 genotypes correlated with reduced SNCA 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 Dementia Screening Interview 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 SNCA 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 SNCA has a dual, opposing, and time-dependent role. This may have implications for the development of therapies that target SNCA expression.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24656894</PMID><DateCreated><Year>2014</Year><Month>05</Month><Day>19</Day></DateCreated><DateCompleted><Year>2015</Year><Month>01</Month><Day>14</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-5126</ISSN><JournalIssue CitedMedium="Internet"><Volume>20</Volume><Issue>6</Issue><PubDate><Year>2014</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Parkinsonism & related disorders</Title><ISOAbbreviation>Parkinsonism Relat. Disord.</ISOAbbreviation></Journal><ArticleTitle>Does α-synuclein have a dual and opposing effect in preclinical vs. clinical Parkinson's disease?</ArticleTitle><Pagination><MedlinePgn>584-9; discussion 584</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.parkreldis.2014.02.021</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1353-8020(14)00074-1</ELocationID><Abstract><AbstractText>α-Synuclein gene (SNCA) multiplications cause familial parkinsonism and allele-length polymorphisms within the SNCA dinucleotide repeat REP1 increase the risk for developing Parkinson's disease (PD). Since SNCA multiplications increase SNCA expression, and REP1 genotypes that increase the risk of developing PD show increased SNCA expression in cell-culture systems, animal models, and human blood and brain, PD therapies seek to reduce SNCA expression. We conducted an observational study of 1098 PD cases to test the hypothesis that REP1 genotypes correlated with reduced SNCA 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 Dementia Screening Interview 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 SNCA 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 SNCA has a dual, opposing, and time-dependent role. This may have implications for the development of therapies that target SNCA expression.</AbstractText><CopyrightInformation>Copyright © 2014 The Authors. Published by Elsevier Ltd.. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Markopoulou</LastName><ForeName>Katerina</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Neurology, NorthShore University HealthSystem, Evanston, IL, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Biernacka</LastName><ForeName>Joanna M</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Armasu</LastName><ForeName>Sebastian M</ForeName><Initials>SM</Initials><AffiliationInfo><Affiliation>Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Anderson</LastName><ForeName>Kari J</ForeName><Initials>KJ</Initials><AffiliationInfo><Affiliation>Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ahlskog</LastName><ForeName>J Eric</ForeName><Initials>JE</Initials><AffiliationInfo><Affiliation>Department of Neurology, Mayo Clinic, Rochester, MN, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chase</LastName><ForeName>Bruce A</ForeName><Initials>BA</Initials><AffiliationInfo><Affiliation>Department of Biology, University of Nebraska at Omaha, Omaha, NE, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chung</LastName><ForeName>Sun Ju</ForeName><Initials>SJ</Initials><AffiliationInfo><Affiliation>Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cunningham</LastName><ForeName>Julie M</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Farrer</LastName><ForeName>Matthew</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Centre for Applied Neurogenetics, University of British Columbia, Vancouver, BC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Frigerio</LastName><ForeName>Roberta</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Neurology, NorthShore University HealthSystem, Evanston, IL, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Maraganore</LastName><ForeName>Demetrius M</ForeName><Initials>DM</Initials><AffiliationInfo><Affiliation>Department of Neurology, NorthShore University HealthSystem, Evanston, IL, USA. Electronic address: dmaraganore@northshore.org.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 ES010751</GrantID><Acronym>ES</Acronym><Agency>NIEHS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R15 NS043162</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>2R01ES10751</GrantID><Acronym>ES</Acronym><Agency>NIEHS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R15NS043162-01A2</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>03</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Parkinsonism Relat Disord</MedlineTA><NlmUniqueID>9513583</NlmUniqueID><ISSNLinking>1353-8020</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C497604">SNCA protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051844">alpha-Synuclein</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Hum Mol Genet. 2001 Dec 15;10(26):3101-9</RefSource><PMID Version="1">11751692</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>JAMA. 2006 Aug 9;296(6):661-70</RefSource><PMID Version="1">16896109</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>PLoS One. 2009;4(10):e7480</RefSource><PMID 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