Characteristics of familial aggregation in early‐onset Alzheimer's disease: Evidence of subgroups
Identifieur interne : 002E87 ( Main/Corpus ); précédent : 002E86; suivant : 002E88Characteristics of familial aggregation in early‐onset Alzheimer's disease: Evidence of subgroups
Auteurs : Campion ; M. Martinez ; D. Hannequin ; A. Brice ; C. Thomas-Anterion ; A. Michon ; M. C. Babron ; B. Dubois ; Y. Goas ; A. Jaillard-Serradt ; F. Ledoze ; F. Pasquier ; M. Puel ; M. A. Zimmerman ; M. Bellis ; J. Mallet ; Y. Agid ; F. Clerget-DarpouxSource :
- American Journal of Medical Genetics [ 0148-7299 ] ; 1995-06-19.
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- KwdEn :
Abstract
Characteristics of familial aggregation of Alzheimer's Disease were studied in 92 families ascertained through a clinically diagnosed proband with an onset below age 60 years. In each family data were systematically collected on the sibships of the proband, of his father, and of his mother. A total of 926 relatives were included and 81% of the living relatives (i.e., 251 individuals) were directly examined. The estimated cumulative risk among first degree relatives was equal to 35% by age 89 years (95% confidence interval 22 to 47%). This result does not support the hypothesis that an autosomal dominant gene, fully penetrant by age 90 years, is segregating within all these pedigrees. Despite the fact that all probands were selected for an onset before age 60 years it was shown that two types of families could be delineated with respect to age at onset among affected relatives: all secondary cases with an onset below age 60 years were contributed by a particular group of families (type 1 families), whereas all secondary cases with an onset after age 60 years were contributed by another group of families (type 2 families). Although genetic interpretation of these findings is not straightforward, they support the hypothesis of etiologic heterogeneity in the determinism of early‐onset Alzheimer's disease. © 1995 Wiley‐Liss, Inc.
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DOI: 10.1002/ajmg.1320600310
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Ledoze</name><affiliation><mods:affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, France</mods:affiliation></affiliation></author><author><name sortKey="Pasquier, F" sort="Pasquier, F" uniqKey="Pasquier F" first="F." last="Pasquier">F. Pasquier</name><affiliation><mods:affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, France</mods:affiliation></affiliation></author><author><name sortKey="Puel, M" sort="Puel, M" uniqKey="Puel M" first="M." last="Puel">M. Puel</name><affiliation><mods:affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, France</mods:affiliation></affiliation></author><author><name sortKey="Zimmerman, M A" sort="Zimmerman, M A" uniqKey="Zimmerman M" first="M. A." last="Zimmerman">M. A. Zimmerman</name><affiliation><mods:affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, France</mods:affiliation></affiliation></author><author><name sortKey="Bellis, M" sort="Bellis, M" uniqKey="Bellis M" first="M." last="Bellis">M. Bellis</name><affiliation><mods:affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, France</mods:affiliation></affiliation></author><author><name sortKey="Mallet, J" sort="Mallet, J" uniqKey="Mallet J" first="J." last="Mallet">J. Mallet</name><affiliation><mods:affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, France</mods:affiliation></affiliation></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y." last="Agid">Y. Agid</name><affiliation><mods:affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, INSERM U 289, France</mods:affiliation></affiliation></author><author><name sortKey="Clerget Arpoux, F" sort="Clerget Arpoux, F" uniqKey="Clerget Arpoux F" first="F." last="Clerget-Darpoux">F. Clerget-Darpoux</name><affiliation><mods:affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, INSERM U155, France</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">American Journal of Medical Genetics</title><title level="j" type="abbrev">Am. J. Med. Genet.</title><idno type="ISSN">0148-7299</idno><idno type="eISSN">1096-8628</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><date type="published" when="1995-06-19">1995-06-19</date><biblScope unit="volume">60</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="221">221</biblScope><biblScope unit="page" to="227">227</biblScope></imprint><idno type="ISSN">0148-7299</idno></series><idno type="istex">C9095FC80509EA62229B8B65A39BF027903D3B8C</idno><idno type="DOI">10.1002/ajmg.1320600310</idno><idno type="ArticleID">AJMG1320600310</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0148-7299</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Alzheimer's disease</term><term>early onset</term><term>morbid risk</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Characteristics of familial aggregation of Alzheimer's Disease were studied in 92 families ascertained through a clinically diagnosed proband with an onset below age 60 years. In each family data were systematically collected on the sibships of the proband, of his father, and of his mother. A total of 926 relatives were included and 81% of the living relatives (i.e., 251 individuals) were directly examined. The estimated cumulative risk among first degree relatives was equal to 35% by age 89 years (95% confidence interval 22 to 47%). This result does not support the hypothesis that an autosomal dominant gene, fully penetrant by age 90 years, is segregating within all these pedigrees. Despite the fact that all probands were selected for an onset before age 60 years it was shown that two types of families could be delineated with respect to age at onset among affected relatives: all secondary cases with an onset below age 60 years were contributed by a particular group of families (type 1 families), whereas all secondary cases with an onset after age 60 years were contributed by another group of families (type 2 families). Although genetic interpretation of these findings is not straightforward, they support the hypothesis of etiologic heterogeneity in the determinism of early‐onset Alzheimer's disease. © 1995 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Dr. Campion</name><affiliations><json:string>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, France</json:string></affiliations></json:item><json:item><name>M. Martinez</name><affiliations><json:string>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, INSERM U155, France</json:string></affiliations></json:item><json:item><name>D. Hannequin</name><affiliations><json:string>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHU Rouen France</json:string></affiliations></json:item><json:item><name>A. Brice</name><affiliations><json:string>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, INSERM U 289, France</json:string></affiliations></json:item><json:item><name>C. Thomas‐Anterion</name><affiliations><json:string>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHU St Etienne, France</json:string></affiliations></json:item><json:item><name>A. Michon</name><affiliations><json:string>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, INSERM U 289, France</json:string></affiliations></json:item><json:item><name>M. C. Babron</name><affiliations><json:string>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, INSERM U155, France</json:string></affiliations></json:item><json:item><name>B. Dubois</name><affiliations><json:string>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, INSERM U 289, France</json:string></affiliations></json:item><json:item><name>Y. Goas</name><affiliations><json:string>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, France</json:string></affiliations></json:item><json:item><name>A. Jaillard‐Serradt</name><affiliations><json:string>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, France</json:string></affiliations></json:item><json:item><name>F. Ledoze</name><affiliations><json:string>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, France</json:string></affiliations></json:item><json:item><name>F. Pasquier</name><affiliations><json:string>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, France</json:string></affiliations></json:item><json:item><name>M. Puel</name><affiliations><json:string>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, France</json:string></affiliations></json:item><json:item><name>M. A. Zimmerman</name><affiliations><json:string>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, France</json:string></affiliations></json:item><json:item><name>M. Bellis</name><affiliations><json:string>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, France</json:string></affiliations></json:item><json:item><name>J. Mallet</name><affiliations><json:string>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, France</json:string></affiliations></json:item><json:item><name>Y. Agid</name><affiliations><json:string>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, INSERM U 289, France</json:string></affiliations></json:item><json:item><name>F. Clerget‐Darpoux</name><affiliations><json:string>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, INSERM U155, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Alzheimer's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>morbid risk</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>early onset</value></json:item></subject><articleId><json:string>AJMG1320600310</json:string></articleId><language><json:string>eng</json:string></language><abstract>Characteristics of familial aggregation of Alzheimer's Disease were studied in 92 families ascertained through a clinically diagnosed proband with an onset below age 60 years. In each family data were systematically collected on the sibships of the proband, of his father, and of his mother. A total of 926 relatives were included and 81% of the living relatives (i.e., 251 individuals) were directly examined. The estimated cumulative risk among first degree relatives was equal to 35% by age 89 years (95% confidence interval 22 to 47%). This result does not support the hypothesis that an autosomal dominant gene, fully penetrant by age 90 years, is segregating within all these pedigrees. Despite the fact that all probands were selected for an onset before age 60 years it was shown that two types of families could be delineated with respect to age at onset among affected relatives: all secondary cases with an onset below age 60 years were contributed by a particular group of families (type 1 families), whereas all secondary cases with an onset after age 60 years were contributed by another group of families (type 2 families). Although genetic interpretation of these findings is not straightforward, they support the hypothesis of etiologic heterogeneity in the determinism of early‐onset Alzheimer's disease. © 1995 Wiley‐Liss, Inc.</abstract><qualityIndicators><score>7.568</score><pdfVersion>1.3</pdfVersion><pdfPageSize>586.8 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>3</keywordCount><abstractCharCount>1346</abstractCharCount><pdfWordCount>5223</pdfWordCount><pdfCharCount>31080</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>214</abstractWordCount></qualityIndicators><title>Characteristics of familial aggregation in early‐onset Alzheimer's disease: Evidence of subgroups</title><genre><json:string>article</json:string></genre><host><volume>60</volume><publisherId><json:string>AJMG</json:string></publisherId><pages><total>7</total><last>227</last><first>221</first></pages><issn><json:string>0148-7299</json:string></issn><issue>3</issue><subject><json:item><value>Article</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1096-8628</json:string></eissn><title>American Journal of Medical Genetics</title><doi><json:string>10.1002/(ISSN)1096-8628</json:string></doi></host><publicationDate>1995</publicationDate><copyrightDate>1995</copyrightDate><doi><json:string>10.1002/ajmg.1320600310</json:string></doi><id>C9095FC80509EA62229B8B65A39BF027903D3B8C</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/C9095FC80509EA62229B8B65A39BF027903D3B8C/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/C9095FC80509EA62229B8B65A39BF027903D3B8C/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/C9095FC80509EA62229B8B65A39BF027903D3B8C/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Characteristics of familial aggregation in early‐onset Alzheimer's disease: Evidence of subgroups</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><availability><p>WILEY</p></availability><date>1995</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Characteristics of familial aggregation in early‐onset Alzheimer's disease: Evidence of subgroups</title><author><persName><surname>Campion</surname></persName><roleName type="degree">Dr.</roleName><note type="correspondence"><p>Correspondence: INSERM U 155, Château de Longchamp, 75016 Paris, France</p></note><affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, France</affiliation></author><author><persName><forename type="first">M.</forename><surname>Martinez</surname></persName><affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, INSERM U155, France</affiliation></author><author><persName><forename type="first">D.</forename><surname>Hannequin</surname></persName><affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHU Rouen France</affiliation></author><author><persName><forename type="first">A.</forename><surname>Brice</surname></persName><affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, INSERM U 289, France</affiliation></author><author><persName><forename type="first">C.</forename><surname>Thomas‐Anterion</surname></persName><affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHU St Etienne, France</affiliation></author><author><persName><forename type="first">A.</forename><surname>Michon</surname></persName><affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, INSERM U 289, France</affiliation></author><author><persName><forename type="first">M. 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In each family data were systematically collected on the sibships of the proband, of his father, and of his mother. A total of 926 relatives were included and 81% of the living relatives (i.e., 251 individuals) were directly examined. The estimated cumulative risk among first degree relatives was equal to 35% by age 89 years (95% confidence interval 22 to 47%). This result does not support the hypothesis that an autosomal dominant gene, fully penetrant by age 90 years, is segregating within all these pedigrees.</p><p>Despite the fact that all probands were selected for an onset before age 60 years it was shown that two types of families could be delineated with respect to age at onset among affected relatives: all secondary cases with an onset below age 60 years were contributed by a particular group of families (type 1 families), whereas all secondary cases with an onset after age 60 years were contributed by another group of families (type 2 families). Although genetic interpretation of these findings is not straightforward, they support the hypothesis of etiologic heterogeneity in the determinism of early‐onset Alzheimer's disease. © 1995 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Characteristics of familial aggregation in early‐onset Alzheimer's disease: Evidence of subgroups</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Familial Aggregation in Alzheimer's Disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Characteristics of familial aggregation in early‐onset Alzheimer's disease: Evidence of subgroups</title></titleInfo><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Campion</namePart><affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, France</affiliation><description>Correspondence: INSERM U 155, Château de Longchamp, 75016 Paris, France</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Martinez</namePart><affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, INSERM U155, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D.</namePart><namePart type="family">Hannequin</namePart><affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHU Rouen France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Brice</namePart><affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, INSERM U 289, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C.</namePart><namePart type="family">Thomas‐Anterion</namePart><affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHU St Etienne, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Michon</namePart><affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, INSERM U 289, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M. 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A.</namePart><namePart type="family">Zimmerman</namePart><affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Bellis</namePart><affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Mallet</namePart><affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y.</namePart><namePart type="family">Agid</namePart><affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, INSERM U 289, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F.</namePart><namePart type="family">Clerget‐Darpoux</namePart><affiliation>Unité de Recherche d'Epidémiologie Génétique (INSERM U 155) Paris, CHR Rouen, INSERM U155, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">1995-06-19</dateIssued><dateCaptured encoding="w3cdtf">1994-03-08</dateCaptured><copyrightDate encoding="w3cdtf">1995</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">5</extent><extent unit="tables">2</extent><extent unit="references">58</extent></physicalDescription><abstract lang="en">Characteristics of familial aggregation of Alzheimer's Disease were studied in 92 families ascertained through a clinically diagnosed proband with an onset below age 60 years. In each family data were systematically collected on the sibships of the proband, of his father, and of his mother. A total of 926 relatives were included and 81% of the living relatives (i.e., 251 individuals) were directly examined. The estimated cumulative risk among first degree relatives was equal to 35% by age 89 years (95% confidence interval 22 to 47%). This result does not support the hypothesis that an autosomal dominant gene, fully penetrant by age 90 years, is segregating within all these pedigrees. Despite the fact that all probands were selected for an onset before age 60 years it was shown that two types of families could be delineated with respect to age at onset among affected relatives: all secondary cases with an onset below age 60 years were contributed by a particular group of families (type 1 families), whereas all secondary cases with an onset after age 60 years were contributed by another group of families (type 2 families). Although genetic interpretation of these findings is not straightforward, they support the hypothesis of etiologic heterogeneity in the determinism of early‐onset Alzheimer's disease. © 1995 Wiley‐Liss, Inc.</abstract><subject lang="en"><genre>Keywords</genre><topic>Alzheimer's disease</topic><topic>morbid risk</topic><topic>early onset</topic></subject><relatedItem type="host"><titleInfo><title>American Journal of Medical Genetics</title></titleInfo><titleInfo type="abbreviated"><title>Am. J. Med. Genet.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Article</topic></subject><identifier type="ISSN">0148-7299</identifier><identifier type="eISSN">1096-8628</identifier><identifier type="DOI">10.1002/(ISSN)1096-8628</identifier><identifier type="PublisherID">AJMG</identifier><part><date>1995</date><detail type="volume"><caption>vol.</caption><number>60</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>221</start><end>227</end><total>7</total></extent></part></relatedItem><identifier type="istex">C9095FC80509EA62229B8B65A39BF027903D3B8C</identifier><identifier type="DOI">10.1002/ajmg.1320600310</identifier><identifier type="ArticleID">AJMG1320600310</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1995 Wiley‐Liss, Inc., A Wiley Company</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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