No Genetic Overlap Between Circulating Iron Levels and Alzheimer's Disease.
Identifieur interne : 001280 ( PubMed/Curation ); précédent : 001279; suivant : 001281No Genetic Overlap Between Circulating Iron Levels and Alzheimer's Disease.
Auteurs : Michelle K. Lupton [Australie] ; Beben Benyamin [Australie] ; Petroula Proitsi [Royaume-Uni] ; Dale R. Nyholt [Australie] ; Manuel A. Ferreira [Australie] ; Grant W. Montgomery [Australie] ; Andrew C. Heath [États-Unis] ; Pamela A. Madden [États-Unis] ; Sarah E. Medland [Australie] ; Scott D. Gordon [Australie] ; Simon Lovestone [Royaume-Uni] ; Magda Tsolaki [Grèce] ; Iwona Kloszewska [Pologne] ; Hilkka Soininen [Finlande] ; Patrizia Mecocci [Italie] ; Bruno Vellas [France] ; John F. Powell [Royaume-Uni] ; Ashley I. Bush [Australie] ; Margaret J. Wright [Australie] ; Nicholas G. Martin [Australie] ; John B. Whitfield [Australie]Source :
- Journal of Alzheimer's disease : JAD [ 1875-8908 ] ; 2017.
Abstract
Iron deposition in the brain is a prominent feature of Alzheimer's disease (AD). Recently, peripheral iron measures have also been shown to be associated with AD status. However, it is not known whether these associations are causal: do elevated or depleted iron levels throughout life have an effect on AD risk? We evaluate the effects of peripheral iron on AD risk using a genetic profile score approach by testing whether variants affecting iron, transferrin, or ferritin levels selected from GWAS meta-analysis of approximately 24,000 individuals are also associated with AD risk in an independent case-control cohort (n∼10,000). Conversely, we test whether AD risk variants from a GWAS meta-analysis of approximately 54,000 account for any variance in iron measures (n∼9,000). We do not identify a genetic relationship, suggesting that peripheral iron is not causal in the initiation of AD pathology.
DOI: 10.3233/JAD-170027
PubMed: 28582860
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<author><name sortKey="Lupton, Michelle K" sort="Lupton, Michelle K" uniqKey="Lupton M" first="Michelle K" last="Lupton">Michelle K. Lupton</name>
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<author><name sortKey="Benyamin, Beben" sort="Benyamin, Beben" uniqKey="Benyamin B" first="Beben" last="Benyamin">Beben Benyamin</name>
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<author><name sortKey="Lovestone, Simon" sort="Lovestone, Simon" uniqKey="Lovestone S" first="Simon" last="Lovestone">Simon Lovestone</name>
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<author><name sortKey="Mecocci, Patrizia" sort="Mecocci, Patrizia" uniqKey="Mecocci P" first="Patrizia" last="Mecocci">Patrizia Mecocci</name>
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<front><div type="abstract" xml:lang="en">Iron deposition in the brain is a prominent feature of Alzheimer's disease (AD). Recently, peripheral iron measures have also been shown to be associated with AD status. However, it is not known whether these associations are causal: do elevated or depleted iron levels throughout life have an effect on AD risk? We evaluate the effects of peripheral iron on AD risk using a genetic profile score approach by testing whether variants affecting iron, transferrin, or ferritin levels selected from GWAS meta-analysis of approximately 24,000 individuals are also associated with AD risk in an independent case-control cohort (n∼10,000). Conversely, we test whether AD risk variants from a GWAS meta-analysis of approximately 54,000 account for any variance in iron measures (n∼9,000). We do not identify a genetic relationship, suggesting that peripheral iron is not causal in the initiation of AD pathology.</div>
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<Title>Journal of Alzheimer's disease : JAD</Title>
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<Abstract><AbstractText>Iron deposition in the brain is a prominent feature of Alzheimer's disease (AD). Recently, peripheral iron measures have also been shown to be associated with AD status. However, it is not known whether these associations are causal: do elevated or depleted iron levels throughout life have an effect on AD risk? We evaluate the effects of peripheral iron on AD risk using a genetic profile score approach by testing whether variants affecting iron, transferrin, or ferritin levels selected from GWAS meta-analysis of approximately 24,000 individuals are also associated with AD risk in an independent case-control cohort (n∼10,000). Conversely, we test whether AD risk variants from a GWAS meta-analysis of approximately 54,000 account for any variance in iron measures (n∼9,000). We do not identify a genetic relationship, suggesting that peripheral iron is not causal in the initiation of AD pathology.</AbstractText>
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<ForeName>Michelle K</ForeName>
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<AffiliationInfo><Affiliation>Institute for Molecular Bioscience, The University of Queensland, Brisbane, QLD, Australia.</Affiliation>
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<Initials>M</Initials>
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<Author ValidYN="Y"><LastName>Wright</LastName>
<ForeName>Margaret J</ForeName>
<Initials>MJ</Initials>
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<AffiliationInfo><Affiliation>Queensland Brain Institute, University of Queensland, Brisbane, Australia.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Centre for Advanced Imaging, University of Queensland, Brisbane, Australia.</Affiliation>
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<Author ValidYN="Y"><LastName>Martin</LastName>
<ForeName>Nicholas G</ForeName>
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<ForeName>John B</ForeName>
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<MedlineJournalInfo><Country>Netherlands</Country>
<MedlineTA>J Alzheimers Dis</MedlineTA>
<NlmUniqueID>9814863</NlmUniqueID>
<ISSNLinking>1387-2877</ISSNLinking>
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<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Alzheimer’s disease</Keyword>
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<Keyword MajorTopicYN="N">dementia</Keyword>
<Keyword MajorTopicYN="N">ferritin</Keyword>
<Keyword MajorTopicYN="N">genetic profile scores</Keyword>
<Keyword MajorTopicYN="N">genome-wide association study</Keyword>
<Keyword MajorTopicYN="N">iron</Keyword>
<Keyword MajorTopicYN="N">population genetics</Keyword>
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