The tau A0 allele in Parkinson's disease.
Identifieur interne : 000501 ( Ncbi/Curation ); précédent : 000500; suivant : 000502The tau A0 allele in Parkinson's disease.
Auteurs : L I Golbe [États-Unis] ; A M Lazzarini ; J R Spychala ; W G Johnson ; E S Stenroos ; M H Mark ; J I SageSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2001.
English descriptors
- KwdEn :
- Aged, Alleles, Case-Control Studies, Female, Gene Frequency, Genetic Markers, Genotype, Humans, Male, Middle Aged, Nerve Tissue Proteins (genetics), Parkinson Disease (classification), Parkinson Disease (genetics), Protein Isoforms, Supranuclear Palsy, Progressive (genetics), Synucleins, tau Proteins (genetics).
- MESH :
- chemical , genetics : Nerve Tissue Proteins, tau Proteins.
- chemical : Genetic Markers, Protein Isoforms, Synucleins.
- classification : Parkinson Disease.
- genetics : Parkinson Disease, Supranuclear Palsy, Progressive.
- Aged, Alleles, Case-Control Studies, Female, Gene Frequency, Genotype, Humans, Male, Middle Aged.
Abstract
Parkinson's disease (PD) is primarily an alpha-synucleinopathy, rather than a tauopathy, but there is evidence for an indirect association of tau with the pathogenetic process in PD. We therefore assessed the frequency in PD of the tau A0 allele, a dinucleotide repeat marker that has been associated with a sporadic tauopathy, progressive supranuclear palsy (PSP). We found the A0 allele to comprise 79.2% of 758 alleles from PD patients and 71.2% of 264 control alleles (P = 0.008). We also performed a meta-analysis of three previous reports, two of which failed to produce statistically significant results. Taken together, they also support a PD/A0 allelic association, even after correction for misdiagnosis of PSP as PD (P< 0.001). The A0/A0 genotype frequency in our patients (62.3%) did not differ significantly from that in controls (53.0%, P = 0.062), but the meta-analysis, even after correction for misdiagnosis, showed a significant result, with P = 0.002. The frequency of A0 allele and the A0/A0 genotype were compatible with Hardy-Weinberg equilibrium. The frequency of the A0 allele and the A0/A0 genotype in our patients with familial PD was not significantly greater than in those with sporadic PD. We conclude that the tau protein may play a small role in the pathogenesis of PD and that biochemical characterization of this role may suggest opportunities for PD prophylaxis.
PubMed: 11391737
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">The tau A0 allele in Parkinson's disease.</title><author><name sortKey="Golbe, L I" sort="Golbe, L I" uniqKey="Golbe L" first="L I" last="Golbe">L I Golbe</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, New Jersey 08901, USA. golbe@umdnj.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, New Jersey 08901</wicri:regionArea><wicri:noRegion>New Jersey 08901</wicri:noRegion></affiliation></author><author><name sortKey="Lazzarini, A M" sort="Lazzarini, A M" uniqKey="Lazzarini A" first="A M" last="Lazzarini">A M Lazzarini</name></author><author><name sortKey="Spychala, J R" sort="Spychala, J R" uniqKey="Spychala J" first="J R" last="Spychala">J R Spychala</name></author><author><name sortKey="Johnson, W G" sort="Johnson, W G" uniqKey="Johnson W" first="W G" last="Johnson">W G Johnson</name></author><author><name sortKey="Stenroos, E S" sort="Stenroos, E S" uniqKey="Stenroos E" first="E S" last="Stenroos">E S Stenroos</name></author><author><name sortKey="Mark, M H" sort="Mark, M H" uniqKey="Mark M" first="M H" last="Mark">M H Mark</name></author><author><name sortKey="Sage, J I" sort="Sage, J I" uniqKey="Sage J" first="J I" last="Sage">J I Sage</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2001">2001</date><idno type="RBID">pubmed:11391737</idno><idno type="pmid">11391737</idno><idno type="wicri:Area/PubMed/Corpus">003D50</idno><idno type="wicri:Area/PubMed/Curation">003D50</idno><idno type="wicri:Area/PubMed/Checkpoint">003C23</idno><idno type="wicri:Area/Ncbi/Merge">000501</idno><idno type="wicri:Area/Ncbi/Curation">000501</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">The tau A0 allele in Parkinson's disease.</title><author><name sortKey="Golbe, L I" sort="Golbe, L I" uniqKey="Golbe L" first="L I" last="Golbe">L I Golbe</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, New Jersey 08901, USA. golbe@umdnj.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, New Jersey 08901</wicri:regionArea><wicri:noRegion>New Jersey 08901</wicri:noRegion></affiliation></author><author><name sortKey="Lazzarini, A M" sort="Lazzarini, A M" uniqKey="Lazzarini A" first="A M" last="Lazzarini">A M Lazzarini</name></author><author><name sortKey="Spychala, J R" sort="Spychala, J R" uniqKey="Spychala J" first="J R" last="Spychala">J R Spychala</name></author><author><name sortKey="Johnson, W G" sort="Johnson, W G" uniqKey="Johnson W" first="W G" last="Johnson">W G Johnson</name></author><author><name sortKey="Stenroos, E S" sort="Stenroos, E S" uniqKey="Stenroos E" first="E S" last="Stenroos">E S Stenroos</name></author><author><name sortKey="Mark, M H" sort="Mark, M H" uniqKey="Mark M" first="M H" last="Mark">M H Mark</name></author><author><name sortKey="Sage, J I" sort="Sage, J I" uniqKey="Sage J" first="J I" last="Sage">J I Sage</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2001" type="published">2001</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Alleles</term><term>Case-Control Studies</term><term>Female</term><term>Gene Frequency</term><term>Genetic Markers</term><term>Genotype</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Nerve Tissue Proteins (genetics)</term><term>Parkinson Disease (classification)</term><term>Parkinson Disease (genetics)</term><term>Protein Isoforms</term><term>Supranuclear Palsy, Progressive (genetics)</term><term>Synucleins</term><term>tau Proteins (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Nerve Tissue Proteins</term><term>tau Proteins</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Genetic Markers</term><term>Protein Isoforms</term><term>Synucleins</term></keywords><keywords scheme="MESH" qualifier="classification" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term><term>Supranuclear Palsy, Progressive</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Alleles</term><term>Case-Control Studies</term><term>Female</term><term>Gene Frequency</term><term>Genotype</term><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is primarily an alpha-synucleinopathy, rather than a tauopathy, but there is evidence for an indirect association of tau with the pathogenetic process in PD. We therefore assessed the frequency in PD of the tau A0 allele, a dinucleotide repeat marker that has been associated with a sporadic tauopathy, progressive supranuclear palsy (PSP). We found the A0 allele to comprise 79.2% of 758 alleles from PD patients and 71.2% of 264 control alleles (P = 0.008). We also performed a meta-analysis of three previous reports, two of which failed to produce statistically significant results. Taken together, they also support a PD/A0 allelic association, even after correction for misdiagnosis of PSP as PD (P< 0.001). The A0/A0 genotype frequency in our patients (62.3%) did not differ significantly from that in controls (53.0%, P = 0.062), but the meta-analysis, even after correction for misdiagnosis, showed a significant result, with P = 0.002. The frequency of A0 allele and the A0/A0 genotype were compatible with Hardy-Weinberg equilibrium. The frequency of the A0 allele and the A0/A0 genotype in our patients with familial PD was not significantly greater than in those with sporadic PD. We conclude that the tau protein may play a small role in the pathogenesis of PD and that biochemical characterization of this role may suggest opportunities for PD prophylaxis.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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