Alcohol dehydrogenase polymorphism and Parkinson's disease.
Identifieur interne : 000250 ( PubMed/Corpus ); précédent : 000249; suivant : 000251Alcohol dehydrogenase polymorphism and Parkinson's disease.
Auteurs : E Tan ; S. Nagamitsu ; T. Matsuura ; M. Khajavi ; J. Jankovic ; W. Ondo ; T. AshizawaSource :
- Neuroscience letters [ 0304-3940 ] ; 2001.
English descriptors
- KwdEn :
- Adult, Aged, Aged, 80 and over, Alcohol Dehydrogenase (genetics), Alleles, Case-Control Studies, Gene Frequency, Genetic Predisposition to Disease, Humans, Huntington Disease (genetics), Isoenzymes (genetics), Linkage Disequilibrium, Middle Aged, Parkinson Disease (genetics), Polymorphism, Genetic (physiology), Reference Values, Tremor (genetics).
- MESH :
- chemical , genetics : Alcohol Dehydrogenase, Isoenzymes.
- genetics : Huntington Disease, Parkinson Disease, Tremor.
- physiology : Polymorphism, Genetic.
- Adult, Aged, Aged, 80 and over, Alleles, Case-Control Studies, Gene Frequency, Genetic Predisposition to Disease, Humans, Linkage Disequilibrium, Middle Aged, Reference Values.
Abstract
A particular alcohol dehydrogenase (ADH) polymorphism (allele A1) in the promoter region of the gene has been recently demonstrated to be associated with increased risk of Parkinson's disease (PD). In a case control study, we examine frequencies of ADH A1 allele in 100 PD patients (i.e. 200 alleles), 100 diseased controls (i.e. 200 alleles), and 194 healthy controls (i.e. 388 alleles). In addition, we study possible association of a combined non-amyloid component of plaque (NACP-Rep 1) allele and ADH A1 allele with risk of PD. There was no statistical significance of the frequencies of ADH A1 allele between PD patients 12/200 (6%), diseased controls 13/200 (6.5%), and healthy controls 20/388 (5.2%). No strong evidence of an association was found between ADH A1 allele and PD susceptibility in our study patients. There was also no suggestion of linkage disequilibrium between NACP-Rep 1 and ADH A1 alleles.
PubMed: 11356310
Links to Exploration step
pubmed:11356310Le document en format XML
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<author><name sortKey="Tan, E K" sort="Tan, E K" uniqKey="Tan E" first="E" last="Tan">E Tan</name>
<affiliation><nlm:affiliation>Department of Neurology, VA Medical Center, Baylor College of Medicine, Houston, TX, USA.</nlm:affiliation>
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<author><name sortKey="Nagamitsu, S" sort="Nagamitsu, S" uniqKey="Nagamitsu S" first="S" last="Nagamitsu">S. Nagamitsu</name>
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<author><name sortKey="Matsuura, T" sort="Matsuura, T" uniqKey="Matsuura T" first="T" last="Matsuura">T. Matsuura</name>
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<author><name sortKey="Khajavi, M" sort="Khajavi, M" uniqKey="Khajavi M" first="M" last="Khajavi">M. Khajavi</name>
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<author><name sortKey="Jankovic, J" sort="Jankovic, J" uniqKey="Jankovic J" first="J" last="Jankovic">J. Jankovic</name>
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<author><name sortKey="Ondo, W" sort="Ondo, W" uniqKey="Ondo W" first="W" last="Ondo">W. Ondo</name>
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<affiliation><nlm:affiliation>Department of Neurology, VA Medical Center, Baylor College of Medicine, Houston, TX, USA.</nlm:affiliation>
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<author><name sortKey="Nagamitsu, S" sort="Nagamitsu, S" uniqKey="Nagamitsu S" first="S" last="Nagamitsu">S. Nagamitsu</name>
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<author><name sortKey="Matsuura, T" sort="Matsuura, T" uniqKey="Matsuura T" first="T" last="Matsuura">T. Matsuura</name>
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<term>Aged</term>
<term>Aged, 80 and over</term>
<term>Alcohol Dehydrogenase (genetics)</term>
<term>Alleles</term>
<term>Case-Control Studies</term>
<term>Gene Frequency</term>
<term>Genetic Predisposition to Disease</term>
<term>Humans</term>
<term>Huntington Disease (genetics)</term>
<term>Isoenzymes (genetics)</term>
<term>Linkage Disequilibrium</term>
<term>Middle Aged</term>
<term>Parkinson Disease (genetics)</term>
<term>Polymorphism, Genetic (physiology)</term>
<term>Reference Values</term>
<term>Tremor (genetics)</term>
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<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Alcohol Dehydrogenase</term>
<term>Isoenzymes</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Huntington Disease</term>
<term>Parkinson Disease</term>
<term>Tremor</term>
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<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Polymorphism, Genetic</term>
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<term>Aged</term>
<term>Aged, 80 and over</term>
<term>Alleles</term>
<term>Case-Control Studies</term>
<term>Gene Frequency</term>
<term>Genetic Predisposition to Disease</term>
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<front><div type="abstract" xml:lang="en">A particular alcohol dehydrogenase (ADH) polymorphism (allele A1) in the promoter region of the gene has been recently demonstrated to be associated with increased risk of Parkinson's disease (PD). In a case control study, we examine frequencies of ADH A1 allele in 100 PD patients (i.e. 200 alleles), 100 diseased controls (i.e. 200 alleles), and 194 healthy controls (i.e. 388 alleles). In addition, we study possible association of a combined non-amyloid component of plaque (NACP-Rep 1) allele and ADH A1 allele with risk of PD. There was no statistical significance of the frequencies of ADH A1 allele between PD patients 12/200 (6%), diseased controls 13/200 (6.5%), and healthy controls 20/388 (5.2%). No strong evidence of an association was found between ADH A1 allele and PD susceptibility in our study patients. There was also no suggestion of linkage disequilibrium between NACP-Rep 1 and ADH A1 alleles.</div>
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<Abstract><AbstractText>A particular alcohol dehydrogenase (ADH) polymorphism (allele A1) in the promoter region of the gene has been recently demonstrated to be associated with increased risk of Parkinson's disease (PD). In a case control study, we examine frequencies of ADH A1 allele in 100 PD patients (i.e. 200 alleles), 100 diseased controls (i.e. 200 alleles), and 194 healthy controls (i.e. 388 alleles). In addition, we study possible association of a combined non-amyloid component of plaque (NACP-Rep 1) allele and ADH A1 allele with risk of PD. There was no statistical significance of the frequencies of ADH A1 allele between PD patients 12/200 (6%), diseased controls 13/200 (6.5%), and healthy controls 20/388 (5.2%). No strong evidence of an association was found between ADH A1 allele and PD susceptibility in our study patients. There was also no suggestion of linkage disequilibrium between NACP-Rep 1 and ADH A1 alleles.</AbstractText>
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