MovDisordV3, PascalFrancis, Corpus, bibRecord, 002A07

The tau A0 allele in Parkinson's disease

Identifieur interne : 002A07 ( PascalFrancis/Corpus ); précédent : 002A06; suivant : 002A08

The tau A0 allele in Parkinson's disease

Auteurs : Lawrence I. Golbe ; Alice M. Lazzarini ; John R. Spychala ; William G. Johnson ; Edward S. Stenroos ; Margery H. Mark ; Jacob I. Sage

Source :

Movement disorders [ 0885-3185 ] ; 2001.

RBID : Pascal:01-0377453

Descripteurs français

Pascal (Inist)
- Parkinson maladie, Réaction chaîne polymérase, Protéine tau, Métaanalyse, Physiopathologie, Homme.

English descriptors

KwdEn :
- Human, Metaanalysis, Parkinson disease, Pathophysiology, Polymerase chain reaction, Tau protein.

Abstract

Parkinson's disease (PD) is primarily an α-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.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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Format Inist (serveur)

NO :	PASCAL 01-0377453 INIST
ET :	The tau A0 allele in Parkinson's disease
AU :	GOLBE (Lawrence I.); LAZZARINI (Alice M.); SPYCHALA (John R.); JOHNSON (William G.); STENROOS (Edward S.); MARK (Margery H.); SAGE (Jacob I.)
AF :	Department of Neurology, UMDNJ-Robert Wood Johnson Medical School/New Brunswick, New Jersey/Etats-Unis (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut.)
DT :	Publication en série; Niveau analytique
SO :	Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2001; Vol. 16; No. 3; Pp. 442-447; Bibl. 22 ref.
LA :	Anglais
EA :	Parkinson's disease (PD) is primarily an α-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.
CC :	002B17G
FD :	Parkinson maladie; Réaction chaîne polymérase; Protéine tau; Métaanalyse; Physiopathologie; Homme
FG :	Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Biologie moléculaire
ED :	Parkinson disease; Polymerase chain reaction; Tau protein; Metaanalysis; Pathophysiology; Human
EG :	Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Molecular biology
SD :	Parkinson enfermedad; Reacción cadena polimerasa; Proteína tau; Mataanálisis; Fisiopatología; Hombre
LO :	INIST-20953.354000099011180060
ID :	01-0377453

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Pascal:01-0377453

Le document en format XML

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<front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is primarily an α-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>
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<s1>© 2001 INIST-CNRS. All rights reserved.</s1>
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<fA45><s0>22 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>01-0377453</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Movement disorders</s0>
</fA64>
<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>Parkinson's disease (PD) is primarily an α-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.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B17G</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Parkinson maladie</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Réaction chaîne polymérase</s0>
<s5>04</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Polymerase chain reaction</s0>
<s5>04</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Reacción cadena polimerasa</s0>
<s5>04</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Protéine tau</s0>
<s5>07</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Tau protein</s0>
<s5>07</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Proteína tau</s0>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Métaanalyse</s0>
<s5>16</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Metaanalysis</s0>
<s5>16</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Mataanálisis</s0>
<s5>16</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Physiopathologie</s0>
<s5>17</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Pathophysiology</s0>
<s5>17</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Fisiopatología</s0>
<s5>17</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Homme</s0>
<s5>20</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Human</s0>
<s5>20</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Hombre</s0>
<s5>20</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>41</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Biologie moléculaire</s0>
<s5>45</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Molecular biology</s0>
<s5>45</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Biología molecular</s0>
<s5>45</s5>
</fC07>
<fN21><s1>267</s1>
</fN21>
</pA>
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<server><NO>PASCAL 01-0377453 INIST</NO>
<ET>The tau A0 allele in Parkinson's disease</ET>
<AU>GOLBE (Lawrence I.); LAZZARINI (Alice M.); SPYCHALA (John R.); JOHNSON (William G.); STENROOS (Edward S.); MARK (Margery H.); SAGE (Jacob I.)</AU>
<AF>Department of Neurology, UMDNJ-Robert Wood Johnson Medical School/New Brunswick, New Jersey/Etats-Unis (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2001; Vol. 16; No. 3; Pp. 442-447; Bibl. 22 ref.</SO>
<LA>Anglais</LA>
<EA>Parkinson's disease (PD) is primarily an α-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.</EA>
<CC>002B17G</CC>
<FD>Parkinson maladie; Réaction chaîne polymérase; Protéine tau; Métaanalyse; Physiopathologie; Homme</FD>
<FG>Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Biologie moléculaire</FG>
<ED>Parkinson disease; Polymerase chain reaction; Tau protein; Metaanalysis; Pathophysiology; Human</ED>
<EG>Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Molecular biology</EG>
<SD>Parkinson enfermedad; Reacción cadena polimerasa; Proteína tau; Mataanálisis; Fisiopatología; Hombre</SD>
<LO>INIST-20953.354000099011180060</LO>
<ID>01-0377453</ID>
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</inist>
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	Movement Disorders (revue)
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Movement Disorders (revue)

The tau A0 allele in Parkinson's disease

The tau A0 allele in Parkinson's disease

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