Current status on Alzheimer disease molecular genetics: from past, to present, to future
Identifieur interne : 001254 ( Istex/Corpus ); précédent : 001253; suivant : 001255Current status on Alzheimer disease molecular genetics: from past, to present, to future
Auteurs : Karolien Bettens ; Kristel Sleegers ; Christine Van BroeckhovenSource :
- Human Molecular Genetics [ 0964-6906 ] ; 2010-04-15.
Abstract
Linkage studies, candidate gene and whole-genome association studies have resulted in a tremendous amount of putative risk genes for Alzheimer's disease (AD). Yet, besides the three causal genesamyloid precursor protein and presenilin 1 and 2 genesand one risk gene apolipoprotein E (APOE), no single functional risk variant was identified. Discussing the possible involvement of rare alleles and other types of genetic variants, this review summarizes the current knowledge on the genetic spectrum of AD and integrates different approaches and recent discoveries by genome-wide association studies.
Url:
DOI: 10.1093/hmg/ddq142
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Yet, besides the three causal genesamyloid precursor protein and presenilin 1 and 2 genesand one risk gene apolipoprotein E (APOE), no single functional risk variant was identified. 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Tel: <phone>+32 32651001</phone>; Fax: <fax>+32 32651012</fax>; Email: <email>christine.vanbroeckhoven@molgen.vib-ua.be</email></corresp></author-notes><pub-date pub-type="ppub"><day>15</day><month>4</month><year>2010</year></pub-date><pub-date pub-type="epub"><day>13</day><month>4</month><year>2010</year></pub-date><volume>19</volume><issue>R1</issue><issue-title>Special Review Issue: Molecular Genetic Advances in Neurological Disease</issue-title><fpage>R4</fpage><lpage>R11</lpage><history><date date-type="received"><day>15</day><month>2</month><year>2010</year></date><date date-type="accepted"><day>7</day><month>4</month><year>2010</year></date></history><permissions><copyright-statement>© The Author 2010. Published by Oxford University Press</copyright-statement><copyright-year>2010</copyright-year><license license-type="creative-commons" xlink:href="http://creativecommons.org/licenses/by-nc/2.0/uk/"><p>This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.</p></license></permissions><abstract><p>Linkage studies, candidate gene and whole-genome association studies have resulted in a tremendous amount of putative risk genes for Alzheimer's disease (AD). Yet, besides the three causal genes—amyloid precursor protein and presenilin 1 and 2 genes—and one risk gene apolipoprotein E (<italic>APOE</italic>), no single functional risk variant was identified. Discussing the possible involvement of rare alleles and other types of genetic variants, this review summarizes the current knowledge on the genetic spectrum of AD and integrates different approaches and recent discoveries by genome-wide association studies.</p></abstract></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Current status on Alzheimer disease molecular genetics: from past, to present, to future</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Current status on Alzheimer disease molecular genetics: from past, to present, to future</title></titleInfo><name type="personal"><namePart type="given">Karolien</namePart><namePart type="family">Bettens</namePart><affiliation>Neurodegenerative Brain Diseases Group, Department of Molecular Genetics, VIB and</affiliation><affiliation>Laboratory of Neurogenetics, Institute Born-Bunge, University of Antwerp, Antwerpen, Belgium</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kristel</namePart><namePart type="family">Sleegers</namePart><affiliation>Neurodegenerative Brain Diseases Group, Department of Molecular Genetics, VIB and</affiliation><affiliation>Laboratory of Neurogenetics, Institute Born-Bunge, University of Antwerp, Antwerpen, Belgium</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christine</namePart><namePart type="family">Van Broeckhoven</namePart><affiliation>Neurodegenerative Brain Diseases Group, Department of Molecular Genetics, VIB and</affiliation><affiliation>Laboratory of Neurogenetics, Institute Born-Bunge, University of Antwerp, Antwerpen, Belgium</affiliation><affiliation>E-mail: christine.vanbroeckhoven@molgen.vib-ua.be</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="review-article"></genre><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">2010-04-15</dateIssued><dateCreated encoding="w3cdtf">2010-04-13</dateCreated><copyrightDate encoding="w3cdtf">2010</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>Linkage studies, candidate gene and whole-genome association studies have resulted in a tremendous amount of putative risk genes for Alzheimer's disease (AD). 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