ParkinsonCanadaV1, Main, Exploration, bibRecord, 000A91

Does α-Synuclein Have A Dual and Opposing Effect in Preclinical versus Clinical Parkinson’s Disease?

Identifieur interne : 000A91 ( Main/Exploration ); précédent : 000A90; suivant : 000A92

Does 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.

RBID : PMC:4723426

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 1,098 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-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 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.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4723426

DOI: 10.1016/j.parkreldis.2014.02.021
PubMed: 24656894
PubMed Central: 4723426

Affiliations:

Le document en format XML

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<term>Disability Evaluation</term>
<term>Female</term>
<term>Genotype</term>
<term>Humans</term>
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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>
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<affiliations><list><country><li>Canada</li>
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<name sortKey="Frigerio, Roberta" sort="Frigerio, Roberta" uniqKey="Frigerio R" first="Roberta" last="Frigerio">Roberta Frigerio</name>
<name sortKey="Maraganore, Demetrius M" sort="Maraganore, Demetrius M" uniqKey="Maraganore D" first="Demetrius M." last="Maraganore">Demetrius M. Maraganore</name>
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La maladie de Parkinson au Canada (serveur d'exploration)

Does α-Synuclein Have A Dual and Opposing Effect in Preclinical versus Clinical Parkinson’s Disease?

Does α-Synuclein Have A Dual and Opposing Effect in Preclinical versus Clinical Parkinson’s Disease?

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	La maladie de Parkinson au Canada (serveur d'exploration)
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.