APOE and COMT polymorphisms are complementary biomarkers of status, stability, and transitions in normal aging and early mild cognitive impairment
Identifieur interne : 000B76 ( Main/Exploration ); précédent : 000B75; suivant : 000B77APOE and COMT polymorphisms are complementary biomarkers of status, stability, and transitions in normal aging and early mild cognitive impairment
Auteurs : Roger A. Dixon [Canada] ; Correne A. Decarlo [Canada] ; Stuart W. S. Macdonald [Canada] ; David Vergote [Canada] ; Jack Jhamandas [Canada] ; David Westaway [Canada]Source :
- Frontiers in Aging Neuroscience [ 1663-4365 ] ; 2014.
Abstract
Url:
DOI: 10.3389/fnagi.2014.00236
PubMed: 25249975
PubMed Central: 4155788
Affiliations:
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Le document en format XML
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polymorphisms are complementary biomarkers of status, stability, and transitions in normal aging and early mild cognitive impairment</title>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main"><italic>APOE</italic>
and <italic>COMT</italic>
polymorphisms are complementary biomarkers of status, stability, and transitions in normal aging and early mild cognitive impairment</title>
<author><name sortKey="Dixon, Roger A" sort="Dixon, Roger A" uniqKey="Dixon R" first="Roger A." last="Dixon">Roger A. Dixon</name>
<affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Department of Psychology, University of Alberta</institution>
<country>Edmonton, AB, Canada</country>
</nlm:aff>
<country xml:lang="fr">Canada</country>
<wicri:regionArea></wicri:regionArea>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Neuroscience and Mental Health Institute, University of Alberta</institution>
<country>Edmonton, AB, Canada</country>
</nlm:aff>
<country xml:lang="fr">Canada</country>
<wicri:regionArea></wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Decarlo, Correne A" sort="Decarlo, Correne A" uniqKey="Decarlo C" first="Correne A." last="Decarlo">Correne A. Decarlo</name>
<affiliation wicri:level="1"><nlm:aff id="aff3"><institution>Department of Psychology, University of Victoria</institution>
<country>Victoria, BC, Canada</country>
</nlm:aff>
<country xml:lang="fr">Canada</country>
<wicri:regionArea></wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Macdonald, Stuart W S" sort="Macdonald, Stuart W S" uniqKey="Macdonald S" first="Stuart W. S." last="Macdonald">Stuart W. S. Macdonald</name>
<affiliation wicri:level="1"><nlm:aff id="aff3"><institution>Department of Psychology, University of Victoria</institution>
<country>Victoria, BC, Canada</country>
</nlm:aff>
<country xml:lang="fr">Canada</country>
<wicri:regionArea></wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Vergote, David" sort="Vergote, David" uniqKey="Vergote D" first="David" last="Vergote">David Vergote</name>
<affiliation wicri:level="1"><nlm:aff id="aff4"><institution>Centre for Prions and Protein Folding Diseases, University of Alberta</institution>
<country>Edmonton, AB, Canada</country>
</nlm:aff>
<country xml:lang="fr">Canada</country>
<wicri:regionArea></wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Jhamandas, Jack" sort="Jhamandas, Jack" uniqKey="Jhamandas J" first="Jack" last="Jhamandas">Jack Jhamandas</name>
<affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Neuroscience and Mental Health Institute, University of Alberta</institution>
<country>Edmonton, AB, Canada</country>
</nlm:aff>
<country xml:lang="fr">Canada</country>
<wicri:regionArea></wicri:regionArea>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="aff5"><institution>Department of Medicine (Neurology), University of Alberta</institution>
<country>Edmonton, AB, Canada</country>
</nlm:aff>
<country xml:lang="fr">Canada</country>
<wicri:regionArea></wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Westaway, David" sort="Westaway, David" uniqKey="Westaway D" first="David" last="Westaway">David Westaway</name>
<affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Neuroscience and Mental Health Institute, University of Alberta</institution>
<country>Edmonton, AB, Canada</country>
</nlm:aff>
<country xml:lang="fr">Canada</country>
<wicri:regionArea></wicri:regionArea>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="aff4"><institution>Centre for Prions and Protein Folding Diseases, University of Alberta</institution>
<country>Edmonton, AB, Canada</country>
</nlm:aff>
<country xml:lang="fr">Canada</country>
<wicri:regionArea></wicri:regionArea>
</affiliation>
</author>
</analytic>
<series><title level="j">Frontiers in Aging Neuroscience</title>
<idno type="eISSN">1663-4365</idno>
<imprint><date when="2014">2014</date>
</imprint>
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<front><div type="abstract" xml:lang="en"><p><bold>Objective:</bold>
Research has reported associations among selected genetic susceptibility biomarkers and risk of (a) normal cognitive aging decrements, (b) established mild cognitive impairment (MCI), and (c) sporadic Alzheimer's disease (AD). In focusing on the transitional normal-to-early MCI phase, we examine associations among three theoretically relevant polymorphisms (<italic>APOE [rs429358, rs7412], BDNF [rs6265], COMT [rs4680]</italic>
) and both baseline cognitive status (MCI vs. normal aging) and two-wave (four-year) longitudinal stability or change profiles. The latter included three profiles: (a) stable as normal aging, (b) stable or chronic impairment (MCI-to-MCI), and (c) emergence of impairment (normal-to-MCI).</p>
<p><bold>Method:</bold>
Genotyped older adults (<italic>n</italic>
= 237 at baseline; age range = 64–91; 62% women) from the Victoria Longitudinal Study were examined for (a) independent and interactive associations of three genetic polymorphisms with (b) two objectively classified cognitive status groups (not-impaired controls (NIC) and MCI) at (c) both baseline and across a two-wave (four-year) longitudinal interval.</p>
<p><bold>Results:</bold>
First, logistic regression revealed that the presence of at least one <italic>APOE ε4</italic>
allele (the risk factor for AD) was linked to greater baseline risk of objective MCI. Second, multinomial logistic regression revealed that (a) the presence of an <italic>APOE ε4</italic>
allele was associated with an increased risk of 4-year MCI status stability (chronicity), and (b) the <italic>COMT</italic>
homozygous risk genotype (G/G or Val/Val) was associated with an increased risk of both MCI-to-MCI stability (chronicity) and emerging NIC-to-MCI conversion.</p>
<p><bold>Discussion:</bold>
Both chronicity and emergence of objectively classified early cognitive impairment may be genetically heterogeneous phenomena, with influences from a panel of both normal cognitive aging (<italic>COMT</italic>
) and AD-related (<italic>APOE</italic>
) polymorphisms.</p>
</div>
</front>
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