Association between Alzheimer's disease and the NOS3 gene
Identifieur interne : 00AF29 ( Main/Exploration ); précédent : 00AF28; suivant : 00AF30Association between Alzheimer's disease and the NOS3 gene
Auteurs : Mohammed Dahiyat [Royaume-Uni] ; Alastair Cumming [Royaume-Uni] ; Charles Harrington [Royaume-Uni] ; Claude Wischik [Royaume-Uni] ; John Xuereb [Royaume-Uni] ; Frank Corrigan [Royaume-Uni] ; Gerome Breen [Royaume-Uni] ; Duncan Shaw [Royaume-Uni] ; David St Clair [Royaume-Uni]Source :
- Annals of Neurology [ 0364-5134 ] ; 1999-10.
Abstract
Alzheimer's disease (AD) is the most common form of neurodegenerative disorder of later life. Genetic studies have demonstrated that the apolipoprotein E (ApoE) gene is an important susceptibility locus; however, other environmental and genetic factors operating alone or in combination with ApoE must also be involved. Among candidate genes that may contribute to this residual risk is the endothelial nitric oxide synthase (NOS3) gene. NO release from vascular endothelium accounts in large part for endothelium‐derived relaxing factor bioactivity. Abnormalities of cerebral small vessels occur early in AD, and it has been demonstrated recently that β‐amyloid interacts with endothelial cells in blood vessels to produce an excess of superoxide radicals. We have genotyped 122 cases of early‐onset AD (EOAD) and 317 cases of late‐onset AD (LOAD) as well as 392 controls for a common structural polymorphism Glu/Asp at codon 298 in the NOS3 gene. We find a highly significant enrichment for Glu/Glu homozygotes in LOAD compared with controls. The effect appears to be independent of ApoE status. NOS3 may be a new genetic risk factor for LOAD.
Url:
DOI: 10.1002/1531-8249(199910)46:4<664::AID-ANA18>3.0.CO;2-J
Affiliations:
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Cambridge</wicri:regionArea><wicri:noRegion>Cambridge</wicri:noRegion></affiliation></author><author><name sortKey="Corrigan, Frank" sort="Corrigan, Frank" uniqKey="Corrigan F" first="Frank" last="Corrigan">Frank Corrigan</name><affiliation wicri:level="1"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Argyll and Bute NHS Trust, Lochgilphead, Argyll</wicri:regionArea><wicri:noRegion>Argyll</wicri:noRegion></affiliation></author><author><name sortKey="Breen, Gerome" sort="Breen, Gerome" uniqKey="Breen G" first="Gerome" last="Breen">Gerome Breen</name><affiliation wicri:level="1"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Mental Health, University of Aberdeen Medical School, Aberdeen</wicri:regionArea><wicri:noRegion>Aberdeen</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Molecular and Cell Biology, Institute of Medical Sciences, University of Aberdeen, 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Aberdeen Medical School, Aberdeen AB25 2ZD</wicri:regionArea><wicri:noRegion>Aberdeen AB25 2ZD</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Annals of Neurology</title><title level="j" type="alt">ANNALS OF NEUROLOGY</title><idno type="ISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><imprint><biblScope unit="vol">46</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="664">664</biblScope><biblScope unit="page" to="667">667</biblScope><biblScope unit="page-count">4</biblScope><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="1999-10">1999-10</date></imprint><idno type="ISSN">0364-5134</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0364-5134</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Alzheimer's disease (AD) is the most common form of neurodegenerative disorder of later life. Genetic studies have demonstrated that the apolipoprotein E (ApoE) gene is an important susceptibility locus; however, other environmental and genetic factors operating alone or in combination with ApoE must also be involved. Among candidate genes that may contribute to this residual risk is the endothelial nitric oxide synthase (NOS3) gene. NO release from vascular endothelium accounts in large part for endothelium‐derived relaxing factor bioactivity. Abnormalities of cerebral small vessels occur early in AD, and it has been demonstrated recently that β‐amyloid interacts with endothelial cells in blood vessels to produce an excess of superoxide radicals. We have genotyped 122 cases of early‐onset AD (EOAD) and 317 cases of late‐onset AD (LOAD) as well as 392 controls for a common structural polymorphism Glu/Asp at codon 298 in the NOS3 gene. We find a highly significant enrichment for Glu/Glu homozygotes in LOAD compared with controls. The effect appears to be independent of ApoE status. NOS3 may be a new genetic risk factor for LOAD.</div></front></TEI><affiliations><list><country><li>Royaume-Uni</li></country></list><tree><country name="Royaume-Uni"><noRegion><name sortKey="Dahiyat, Mohammed" sort="Dahiyat, Mohammed" uniqKey="Dahiyat M" first="Mohammed" last="Dahiyat">Mohammed Dahiyat</name></noRegion><name sortKey="Breen, Gerome" sort="Breen, Gerome" uniqKey="Breen G" first="Gerome" last="Breen">Gerome Breen</name><name sortKey="Breen, Gerome" sort="Breen, Gerome" uniqKey="Breen G" first="Gerome" last="Breen">Gerome Breen</name><name sortKey="Corrigan, Frank" sort="Corrigan, Frank" uniqKey="Corrigan F" first="Frank" last="Corrigan">Frank Corrigan</name><name sortKey="Cumming, Alastair" sort="Cumming, Alastair" uniqKey="Cumming A" first="Alastair" last="Cumming">Alastair Cumming</name><name sortKey="Dahiyat, Mohammed" sort="Dahiyat, Mohammed" uniqKey="Dahiyat M" first="Mohammed" last="Dahiyat">Mohammed Dahiyat</name><name sortKey="Harrington, Charles" sort="Harrington, Charles" uniqKey="Harrington C" first="Charles" last="Harrington">Charles Harrington</name><name sortKey="Shaw, Duncan" sort="Shaw, Duncan" uniqKey="Shaw D" first="Duncan" last="Shaw">Duncan Shaw</name><name sortKey="St Clair, David" sort="St Clair, David" uniqKey="St Clair D" first="David" last="St Clair">David St Clair</name><name sortKey="St Clair, David" sort="St Clair, David" uniqKey="St Clair D" first="David" last="St Clair">David St Clair</name><name sortKey="Wischik, Claude" sort="Wischik, Claude" uniqKey="Wischik C" first="Claude" last="Wischik">Claude Wischik</name><name sortKey="Xuereb, John" sort="Xuereb, John" uniqKey="Xuereb J" first="John" last="Xuereb">John Xuereb</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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