Polymorphic genes of detoxification and mitochondrial enzymes and risk for progressive supranuclear palsy: a case control study
Identifieur interne : 001151 ( Main/Exploration ); précédent : 001150; suivant : 001152Polymorphic genes of detoxification and mitochondrial enzymes and risk for progressive supranuclear palsy: a case control study
Auteurs : Lisa F. Potts [États-Unis] ; Alex C. Cambon [États-Unis] ; Owen A. Ross [États-Unis] ; Rosa Rademakers [États-Unis] ; Dennis W. Dickson [États-Unis] ; Ryan J. Uitti [États-Unis] ; Zbigniew K. Wszolek [États-Unis] ; Shesh N. Rai [États-Unis] ; Matthew J. Farrer [États-Unis, Canada] ; David W. Hein [États-Unis] ; Irene Litvan [États-Unis]Source :
- BMC Medical Genetics [ 1471-2350 ] ; 2012.
Abstract
There are no known causes for progressive supranuclear palsy (PSP). The
DNA from 553 autopsy-confirmed Caucasian PSP cases (266 females, 279 males; age at onset 68 ± 8 years; age at death 75 ± 8) from the Society for PSP Brain Bank and 425 clinical control samples (197 females, 226 males; age at draw 72 ± 11 years) from healthy volunteers were genotyped using Taqman PCR and the SequenomiPLEX Gold assay.
The proportion of NAT2 rapid acetylators compared to intermediate and slow acetylators was larger in cases than in controls (OR = 1.82, p < 0.05). There were no allelic or genotypic associations with PSP for any other SNPs tested with the exception of
Our results show that NAT2 rapid acetylator phenotype is associated with PSP, suggesting that NAT2 may be responsible for activation of a xenobiotic whose metabolite is neurotoxic. Although our results need to be further confirmed in an independent sample, NAT2 acetylation status should be considered in future genetic and epidemiological studies of PSP.
Url:
DOI: 10.1186/1471-2350-13-16
PubMed: 22424094
PubMed Central: 3344705
Affiliations:
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<country xml:lang="fr">Canada</country>
<wicri:regionArea>Department of Medical Genetics, Centre of Applied Neurogenetics, Brain Research Centre, University of British Columbia, Vancouver, British Columbia</wicri:regionArea>
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<author><name sortKey="Hein, David W" sort="Hein, David W" uniqKey="Hein D" first="David W" last="Hein">David W. Hein</name>
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<author><name sortKey="Litvan, Irene" sort="Litvan, Irene" uniqKey="Litvan I" first="Irene" last="Litvan">Irene Litvan</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Anatomical Sciences and Neurobiology, University of Louisville, Louisville, KY</wicri:regionArea>
<wicri:noRegion>KY</wicri:noRegion>
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<affiliation wicri:level="1"><nlm:aff id="I8">Department of Neurology, University of Louisville, Louisville, KY, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Neurology, University of Louisville, Louisville, KY</wicri:regionArea>
<wicri:noRegion>KY</wicri:noRegion>
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<affiliation wicri:level="1"><nlm:aff id="I9">Department of Neurosciences, University of California San Diego, La Jolla, CA, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Neurosciences, University of California San Diego, La Jolla, CA</wicri:regionArea>
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<front><div type="abstract" xml:lang="en"><sec><title>Background</title>
<p>There are no known causes for progressive supranuclear palsy (PSP). The <italic>microtubule associated protein tau </italic>
(<italic>MAPT) </italic>
H1 haplotype is the major genetic factor associated with risk of PSP, with both oxidative stress and mitochondrial dysfunction also implicated. We investigated whether specific single nucleotide polymorphisms (SNPs) in genes encoding enzymes of xenobiotic detoxification, mitochondrial functioning, or oxidative stress response, including <italic>debrisoquine 4-hydroxylase, paraoxonase 1 </italic>
and <italic>2, N-acetyltransferase 1 </italic>
and <italic>2 (NAT2), superoxide dismutase 1 </italic>
and <italic>2, and PTEN-induced putative kinase </italic>
are associated with PSP.</p>
</sec>
<sec><title>Methods</title>
<p>DNA from 553 autopsy-confirmed Caucasian PSP cases (266 females, 279 males; age at onset 68 ± 8 years; age at death 75 ± 8) from the Society for PSP Brain Bank and 425 clinical control samples (197 females, 226 males; age at draw 72 ± 11 years) from healthy volunteers were genotyped using Taqman PCR and the SequenomiPLEX Gold assay.</p>
</sec>
<sec><title>Results</title>
<p>The proportion of NAT2 rapid acetylators compared to intermediate and slow acetylators was larger in cases than in controls (OR = 1.82, p < 0.05). There were no allelic or genotypic associations with PSP for any other SNPs tested with the exception of <italic>MAPT </italic>
(p < 0.001).</p>
</sec>
<sec><title>Conclusions</title>
<p>Our results show that NAT2 rapid acetylator phenotype is associated with PSP, suggesting that NAT2 may be responsible for activation of a xenobiotic whose metabolite is neurotoxic. Although our results need to be further confirmed in an independent sample, NAT2 acetylation status should be considered in future genetic and epidemiological studies of PSP.</p>
</sec>
</div>
</front>
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