Absence of Duplication of Chromosome 21 Genes in Familial and Sporadic Alzheimer's Disease
The possibility that Alzheimer's disease (AD) is caused by overexpression or duplication of one or more genes on chromosome 21 has been raised by the observation of AD-like neuropathologic changes in individuals with Down syndrome and by the mapping of both the defect for familial AD and the am...
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| Veröffentlicht in: | Science (American Association for the Advancement of Science) 1987-10, Vol.238 (4827), p.664-666 |
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| creator | St George-Hyslop, Peter H. Tanzi, Rudolph E. Polinsky, Ronald J. Neve, Rachael L. Pollen, Daniel Drachman, David Growdon, John Cupples, L. Adrienne Nee, Linda Myers, Richard H. O'Sullivan, Dianne Watkins, Paul C. Amos, Jean A. Deutsch, Curtis K. Bodfish, James W. Kinsbourne, Marcel Feldman, Robert G. Bruni, Amalia Amaducci, Luigi Foncin, Jean-Francois Gusella, James F. |
| description | The possibility that Alzheimer's disease (AD) is caused by overexpression or duplication of one or more genes on chromosome 21 has been raised by the observation of AD-like neuropathologic changes in individuals with Down syndrome and by the mapping of both the defect for familial AD and the amyloid β protein gene to this autosome. Possible duplication on chromosome 21 was investigated in both familial and sporadic AD by means of restriction fragment length polymorphisms for the amyloid and SODI loci, as well as for DNA markers in the vicinity of the familial AD defect and in the critical Down syndrome region of chromosome 21. No evidence of increased DNA dosage was observed in either brain or leukocytes of patients with inherited or sporadic forms of AD. Duplication of these regions is therefore not a frequent event in either form of AD. Furthermore, no significant allelic association was detected between AD and any of the loci, including the amyloid and SODI genes, providing no support for the hypothesis that defects in these specific genes are the primary cause of AD. |
| doi_str_mv | 10.1126/science.2890206 |
| format | Article |
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Adrienne ; Nee, Linda ; Myers, Richard H. ; O'Sullivan, Dianne ; Watkins, Paul C. ; Amos, Jean A. ; Deutsch, Curtis K. ; Bodfish, James W. ; Kinsbourne, Marcel ; Feldman, Robert G. ; Bruni, Amalia ; Amaducci, Luigi ; Foncin, Jean-Francois ; Gusella, James F.</creator><creatorcontrib>St George-Hyslop, Peter H. ; Tanzi, Rudolph E. ; Polinsky, Ronald J. ; Neve, Rachael L. ; Pollen, Daniel ; Drachman, David ; Growdon, John ; Cupples, L. Adrienne ; Nee, Linda ; Myers, Richard H. ; O'Sullivan, Dianne ; Watkins, Paul C. ; Amos, Jean A. ; Deutsch, Curtis K. ; Bodfish, James W. ; Kinsbourne, Marcel ; Feldman, Robert G. ; Bruni, Amalia ; Amaducci, Luigi ; Foncin, Jean-Francois ; Gusella, James F.</creatorcontrib><description>The possibility that Alzheimer's disease (AD) is caused by overexpression or duplication of one or more genes on chromosome 21 has been raised by the observation of AD-like neuropathologic changes in individuals with Down syndrome and by the mapping of both the defect for familial AD and the amyloid β protein gene to this autosome. Possible duplication on chromosome 21 was investigated in both familial and sporadic AD by means of restriction fragment length polymorphisms for the amyloid and SODI loci, as well as for DNA markers in the vicinity of the familial AD defect and in the critical Down syndrome region of chromosome 21. No evidence of increased DNA dosage was observed in either brain or leukocytes of patients with inherited or sporadic forms of AD. Duplication of these regions is therefore not a frequent event in either form of AD. Furthermore, no significant allelic association was detected between AD and any of the loci, including the amyloid and SODI genes, providing no support for the hypothesis that defects in these specific genes are the primary cause of AD.</description><identifier>ISSN: 0036-8075</identifier><identifier>EISSN: 1095-9203</identifier><identifier>DOI: 10.1126/science.2890206</identifier><identifier>PMID: 2890206</identifier><identifier>CODEN: SCIEAS</identifier><language>eng</language><publisher>Washington, DC: The American Association for the Advancement of Science</publisher><subject>Alleles ; Alzheimer Disease - genetics ; Alzheimer's disease ; Amyloid - genetics ; Amyloids ; Biological and medical sciences ; Chromosomes ; Chromosomes, Human, Pair 21 ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; DNA ; DNA probes ; Gene dosage ; Genes ; Genetic aspects ; Genetic Linkage ; Genetic loci ; Genetics ; Human chromosome 21 ; Humans ; Leukocytes ; Medical genetics ; Medical research ; Medical schools ; Medical sciences ; Neurology ; Polymorphism, Restriction Fragment Length</subject><ispartof>Science (American Association for the Advancement of Science), 1987-10, Vol.238 (4827), p.664-666</ispartof><rights>Copyright 1987 The American Association for the Advancement of Science</rights><rights>1988 INIST-CNRS</rights><rights>COPYRIGHT 1987 American Association for the Advancement of Science</rights><rights>COPYRIGHT 1987 American Association for the Advancement of Science</rights><rights>Copyright American Association for the Advancement of Science Oct 30, 1987</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c698t-cfe592db2c52fb3afcf88645a91ee23e687e073f2881ea1d3a57a0bdfb60fa7c3</citedby><cites>FETCH-LOGICAL-c698t-cfe592db2c52fb3afcf88645a91ee23e687e073f2881ea1d3a57a0bdfb60fa7c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/1700485$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/1700485$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,776,780,799,2870,2871,27903,27904,57995,58228</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=7455130$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2890206$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>St George-Hyslop, Peter H.</creatorcontrib><creatorcontrib>Tanzi, Rudolph E.</creatorcontrib><creatorcontrib>Polinsky, Ronald J.</creatorcontrib><creatorcontrib>Neve, Rachael L.</creatorcontrib><creatorcontrib>Pollen, Daniel</creatorcontrib><creatorcontrib>Drachman, David</creatorcontrib><creatorcontrib>Growdon, John</creatorcontrib><creatorcontrib>Cupples, L. Adrienne</creatorcontrib><creatorcontrib>Nee, Linda</creatorcontrib><creatorcontrib>Myers, Richard H.</creatorcontrib><creatorcontrib>O'Sullivan, Dianne</creatorcontrib><creatorcontrib>Watkins, Paul C.</creatorcontrib><creatorcontrib>Amos, Jean A.</creatorcontrib><creatorcontrib>Deutsch, Curtis K.</creatorcontrib><creatorcontrib>Bodfish, James W.</creatorcontrib><creatorcontrib>Kinsbourne, Marcel</creatorcontrib><creatorcontrib>Feldman, Robert G.</creatorcontrib><creatorcontrib>Bruni, Amalia</creatorcontrib><creatorcontrib>Amaducci, Luigi</creatorcontrib><creatorcontrib>Foncin, Jean-Francois</creatorcontrib><creatorcontrib>Gusella, James F.</creatorcontrib><title>Absence of Duplication of Chromosome 21 Genes in Familial and Sporadic Alzheimer's Disease</title><title>Science (American Association for the Advancement of Science)</title><addtitle>Science</addtitle><description>The possibility that Alzheimer's disease (AD) is caused by overexpression or duplication of one or more genes on chromosome 21 has been raised by the observation of AD-like neuropathologic changes in individuals with Down syndrome and by the mapping of both the defect for familial AD and the amyloid β protein gene to this autosome. Possible duplication on chromosome 21 was investigated in both familial and sporadic AD by means of restriction fragment length polymorphisms for the amyloid and SODI loci, as well as for DNA markers in the vicinity of the familial AD defect and in the critical Down syndrome region of chromosome 21. No evidence of increased DNA dosage was observed in either brain or leukocytes of patients with inherited or sporadic forms of AD. Duplication of these regions is therefore not a frequent event in either form of AD. Furthermore, no significant allelic association was detected between AD and any of the loci, including the amyloid and SODI genes, providing no support for the hypothesis that defects in these specific genes are the primary cause of AD.</description><subject>Alleles</subject><subject>Alzheimer Disease - genetics</subject><subject>Alzheimer's disease</subject><subject>Amyloid - genetics</subject><subject>Amyloids</subject><subject>Biological and medical sciences</subject><subject>Chromosomes</subject><subject>Chromosomes, Human, Pair 21</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>DNA</subject><subject>DNA probes</subject><subject>Gene dosage</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic Linkage</subject><subject>Genetic loci</subject><subject>Genetics</subject><subject>Human chromosome 21</subject><subject>Humans</subject><subject>Leukocytes</subject><subject>Medical genetics</subject><subject>Medical research</subject><subject>Medical schools</subject><subject>Medical sciences</subject><subject>Neurology</subject><subject>Polymorphism, Restriction Fragment Length</subject><issn>0036-8075</issn><issn>1095-9203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1987</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqN0s1v0zAUAPAIgUYZnLmAFE2IHUY3f9SJcywdK5Mqehhw4BK9OM-dKycudiIBfz2uGm0DVVrlg2W_n9-T7Zckryk5p5RlF0EZbBWeM1kQRrInyYiSQowLRvjTZEQIz8aS5OJ58iKENSExVvCj5Gjgo-THtArbBKnT6WW_sUZBZ1y7Xc5uvWtccA2mjKZzbDGkpk2voDHWgE2hrdObjfNQG5VO7Z9bNA3605BemoAQ8GXyTIMN-GqYj5NvV5--zj6PF8v59Wy6GKuskN1YaRQFqyumBNMVB620lNlEQEERGcdM5khyrpmUFIHWHEQOpKp1lRENueLHyftd3o13P3sMXdmYoNBaaNH1oZSUSC5Z9ijkgsgJkcWjkFEqac7zCE_-g2vX-zbeNhoumMwLGtHZDq3AYmla7ToPahXf04N1LWoTt6dZLCyybe0Pe3QcNTZG7eGn__AoOvzVraAPoby--XKoXH4_VH6cHyjlfPFQnu2TylmLKyxjQ8yWD_XFTivvQvCoy403DfjfJSXltu_Loe_LoZHjibfDT_RVg_Wdv4-_G-IQFFjtoVUm3LF8IgTlJLI3O7YOnfP3VXNCJlLwv7x7EFo</recordid><startdate>19871030</startdate><enddate>19871030</enddate><creator>St George-Hyslop, Peter H.</creator><creator>Tanzi, Rudolph E.</creator><creator>Polinsky, Ronald J.</creator><creator>Neve, Rachael L.</creator><creator>Pollen, Daniel</creator><creator>Drachman, David</creator><creator>Growdon, John</creator><creator>Cupples, L. 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Adrienne</au><au>Nee, Linda</au><au>Myers, Richard H.</au><au>O'Sullivan, Dianne</au><au>Watkins, Paul C.</au><au>Amos, Jean A.</au><au>Deutsch, Curtis K.</au><au>Bodfish, James W.</au><au>Kinsbourne, Marcel</au><au>Feldman, Robert G.</au><au>Bruni, Amalia</au><au>Amaducci, Luigi</au><au>Foncin, Jean-Francois</au><au>Gusella, James F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Absence of Duplication of Chromosome 21 Genes in Familial and Sporadic Alzheimer's Disease</atitle><jtitle>Science (American Association for the Advancement of Science)</jtitle><addtitle>Science</addtitle><date>1987-10-30</date><risdate>1987</risdate><volume>238</volume><issue>4827</issue><spage>664</spage><epage>666</epage><pages>664-666</pages><issn>0036-8075</issn><eissn>1095-9203</eissn><coden>SCIEAS</coden><abstract>The possibility that Alzheimer's disease (AD) is caused by overexpression or duplication of one or more genes on chromosome 21 has been raised by the observation of AD-like neuropathologic changes in individuals with Down syndrome and by the mapping of both the defect for familial AD and the amyloid β protein gene to this autosome. Possible duplication on chromosome 21 was investigated in both familial and sporadic AD by means of restriction fragment length polymorphisms for the amyloid and SODI loci, as well as for DNA markers in the vicinity of the familial AD defect and in the critical Down syndrome region of chromosome 21. No evidence of increased DNA dosage was observed in either brain or leukocytes of patients with inherited or sporadic forms of AD. Duplication of these regions is therefore not a frequent event in either form of AD. Furthermore, no significant allelic association was detected between AD and any of the loci, including the amyloid and SODI genes, providing no support for the hypothesis that defects in these specific genes are the primary cause of AD.</abstract><cop>Washington, DC</cop><pub>The American Association for the Advancement of Science</pub><pmid>2890206</pmid><doi>10.1126/science.2890206</doi><tpages>3</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0036-8075 |
| ispartof | Science (American Association for the Advancement of Science), 1987-10, Vol.238 (4827), p.664-666 |
| issn | 0036-8075 1095-9203 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_81083826 |
| source | American Association for the Advancement of Science; Jstor Complete Legacy; MEDLINE |
| subjects | Alleles Alzheimer Disease - genetics Alzheimer's disease Amyloid - genetics Amyloids Biological and medical sciences Chromosomes Chromosomes, Human, Pair 21 Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases DNA DNA probes Gene dosage Genes Genetic aspects Genetic Linkage Genetic loci Genetics Human chromosome 21 Humans Leukocytes Medical genetics Medical research Medical schools Medical sciences Neurology Polymorphism, Restriction Fragment Length |
| title | Absence of Duplication of Chromosome 21 Genes in Familial and Sporadic Alzheimer's Disease |
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