ApoE genotype accounts for the vast majority of AD risk and AD pathology
In this review, evidence is provided that apolipoprotein E (apoE) genotype accounts for the majority of Alzheimer’s disease (AD) risk and pathology. The three major human isoforms, apoE2, apoE3, and apoE4, are encoded by different alleles (ε2, ε3, ε4) and regulate lipid metabolism and redistribution...
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| Veröffentlicht in: | Neurobiology of aging 2004-05, Vol.25 (5), p.641-650 |
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| creator | Raber, Jacob Huang, Yadong Ashford, J.Wesson |
| description | In this review, evidence is provided that apolipoprotein E (apoE) genotype accounts for the majority of Alzheimer’s disease (AD) risk and pathology. The three major human isoforms, apoE2, apoE3, and apoE4, are encoded by different alleles (ε2, ε3, ε4) and regulate lipid metabolism and redistribution. ApoE isoforms differ in their effects on AD risk and pathology. Clinical and epidemiological data have indicated that the ε4 allele may account for 50% of AD in the United States. Further, the rarity of AD among carriers of the ε2 allele suggests that allelic variations in the gene encoding this protein may account for over 95% of AD cases. ApoE4 disrupts memory function in rodents. Further studies have indicated that fragments of apoE may contribute to both plaque and tangle formation. Thus, the epidemiologic and basic science evidence suggest that apoE genotype accounts for the vast majority of AD risk and pathology. |
| doi_str_mv | 10.1016/j.neurobiolaging.2003.12.023 |
| format | Article |
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The three major human isoforms, apoE2, apoE3, and apoE4, are encoded by different alleles (ε2, ε3, ε4) and regulate lipid metabolism and redistribution. ApoE isoforms differ in their effects on AD risk and pathology. Clinical and epidemiological data have indicated that the ε4 allele may account for 50% of AD in the United States. Further, the rarity of AD among carriers of the ε2 allele suggests that allelic variations in the gene encoding this protein may account for over 95% of AD cases. ApoE4 disrupts memory function in rodents. Further studies have indicated that fragments of apoE may contribute to both plaque and tangle formation. Thus, the epidemiologic and basic science evidence suggest that apoE genotype accounts for the vast majority of AD risk and pathology.</description><identifier>ISSN: 0197-4580</identifier><identifier>EISSN: 1558-1497</identifier><identifier>DOI: 10.1016/j.neurobiolaging.2003.12.023</identifier><identifier>PMID: 15172743</identifier><identifier>CODEN: NEAGDO</identifier><language>eng</language><publisher>London: Elsevier Inc</publisher><subject>AD pathology ; AD risk ; Age Factors ; Alzheimer Disease - epidemiology ; Alzheimer Disease - etiology ; Alzheimer Disease - genetics ; Animals ; ApoE genotype ; Apolipoproteins E - classification ; Apolipoproteins E - genetics ; Apolipoproteins E - metabolism ; Biological and medical sciences ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Disease Models, Animal ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Humans ; Medical sciences ; Memory Disorders - etiology ; Memory Disorders - genetics ; Neurofibrillary Tangles - genetics ; Neurology ; Plaque, Amyloid - genetics ; Risk ; Sex Factors</subject><ispartof>Neurobiology of aging, 2004-05, Vol.25 (5), p.641-650</ispartof><rights>2004 Elsevier Inc.</rights><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c542t-45fd767244b1c243780e1288d161aac4932bd8ce4721de0ba0926c6b9c2884b83</citedby><cites>FETCH-LOGICAL-c542t-45fd767244b1c243780e1288d161aac4932bd8ce4721de0ba0926c6b9c2884b83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.neurobiolaging.2003.12.023$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>309,310,314,780,784,789,790,3548,23929,23930,25139,27923,27924,45994</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15895940$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15172743$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Raber, Jacob</creatorcontrib><creatorcontrib>Huang, Yadong</creatorcontrib><creatorcontrib>Ashford, J.Wesson</creatorcontrib><title>ApoE genotype accounts for the vast majority of AD risk and AD pathology</title><title>Neurobiology of aging</title><addtitle>Neurobiol Aging</addtitle><description>In this review, evidence is provided that apolipoprotein E (apoE) genotype accounts for the majority of Alzheimer’s disease (AD) risk and pathology. The three major human isoforms, apoE2, apoE3, and apoE4, are encoded by different alleles (ε2, ε3, ε4) and regulate lipid metabolism and redistribution. ApoE isoforms differ in their effects on AD risk and pathology. Clinical and epidemiological data have indicated that the ε4 allele may account for 50% of AD in the United States. Further, the rarity of AD among carriers of the ε2 allele suggests that allelic variations in the gene encoding this protein may account for over 95% of AD cases. ApoE4 disrupts memory function in rodents. Further studies have indicated that fragments of apoE may contribute to both plaque and tangle formation. Thus, the epidemiologic and basic science evidence suggest that apoE genotype accounts for the vast majority of AD risk and pathology.</description><subject>AD pathology</subject><subject>AD risk</subject><subject>Age Factors</subject><subject>Alzheimer Disease - epidemiology</subject><subject>Alzheimer Disease - etiology</subject><subject>Alzheimer Disease - genetics</subject><subject>Animals</subject><subject>ApoE genotype</subject><subject>Apolipoproteins E - classification</subject><subject>Apolipoproteins E - genetics</subject><subject>Apolipoproteins E - metabolism</subject><subject>Biological and medical sciences</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Disease Models, Animal</subject><subject>Gene Frequency</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Memory Disorders - etiology</subject><subject>Memory Disorders - genetics</subject><subject>Neurofibrillary Tangles - genetics</subject><subject>Neurology</subject><subject>Plaque, Amyloid - genetics</subject><subject>Risk</subject><subject>Sex Factors</subject><issn>0197-4580</issn><issn>1558-1497</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqN0UGP1CAUB3BiNO64-hUMB914mcqjtEDiZbLuuiabeNEzofR1lrFTKtBN5tvLZCZRL-oJDr_3eI8_IW-AVcCgfb-rJlxi6HwY7dZP24ozVlfAK8brJ2QFTaPWILR8SlYMtFyLRrEL8iKlHWNMCtk-JxfQgORS1Ctyt5nDDd3iFPJhRmqdC8uUEx1CpPkB6aNNme7tLkSfDzQMdPORRp--Uzv1x_ts80MYw_bwkjwb7Jjw1fm8JN9ub75e363vv3z6fL25X7tG8FymGXrZSi5EB46LWiqGwJXqoQVrndA173rlUEgOPbLOMs1b13baFSQ6VV-Sq1PfOYYfC6Zs9j45HEc7YViSkWVn0ba6wHd_haBkoxpZ83_3BNlqUEwW-OEEXQwpRRzMHP3exoMBZo7pmJ35Mx1zTMcANyWdUv76_M7S7bH_VXyOo4C3Z2CTs-MQ7eR8-s0p3WjBirs9OSw__egxmuQ8Tg57H9Fl0wf_fxP9BA5otDU</recordid><startdate>20040501</startdate><enddate>20040501</enddate><creator>Raber, Jacob</creator><creator>Huang, Yadong</creator><creator>Ashford, J.Wesson</creator><general>Elsevier Inc</general><general>Elsevier Science</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>20040501</creationdate><title>ApoE genotype accounts for the vast majority of AD risk and AD pathology</title><author>Raber, Jacob ; Huang, Yadong ; Ashford, J.Wesson</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c542t-45fd767244b1c243780e1288d161aac4932bd8ce4721de0ba0926c6b9c2884b83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>AD pathology</topic><topic>AD risk</topic><topic>Age Factors</topic><topic>Alzheimer Disease - epidemiology</topic><topic>Alzheimer Disease - etiology</topic><topic>Alzheimer Disease - genetics</topic><topic>Animals</topic><topic>ApoE genotype</topic><topic>Apolipoproteins E - classification</topic><topic>Apolipoproteins E - genetics</topic><topic>Apolipoproteins E - metabolism</topic><topic>Biological and medical sciences</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Disease Models, Animal</topic><topic>Gene Frequency</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Memory Disorders - etiology</topic><topic>Memory Disorders - genetics</topic><topic>Neurofibrillary Tangles - genetics</topic><topic>Neurology</topic><topic>Plaque, Amyloid - genetics</topic><topic>Risk</topic><topic>Sex Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Raber, Jacob</creatorcontrib><creatorcontrib>Huang, Yadong</creatorcontrib><creatorcontrib>Ashford, J.Wesson</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neurobiology of aging</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Raber, Jacob</au><au>Huang, Yadong</au><au>Ashford, J.Wesson</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ApoE genotype accounts for the vast majority of AD risk and AD pathology</atitle><jtitle>Neurobiology of aging</jtitle><addtitle>Neurobiol Aging</addtitle><date>2004-05-01</date><risdate>2004</risdate><volume>25</volume><issue>5</issue><spage>641</spage><epage>650</epage><pages>641-650</pages><issn>0197-4580</issn><eissn>1558-1497</eissn><coden>NEAGDO</coden><abstract>In this review, evidence is provided that apolipoprotein E (apoE) genotype accounts for the majority of Alzheimer’s disease (AD) risk and pathology. The three major human isoforms, apoE2, apoE3, and apoE4, are encoded by different alleles (ε2, ε3, ε4) and regulate lipid metabolism and redistribution. ApoE isoforms differ in their effects on AD risk and pathology. Clinical and epidemiological data have indicated that the ε4 allele may account for 50% of AD in the United States. Further, the rarity of AD among carriers of the ε2 allele suggests that allelic variations in the gene encoding this protein may account for over 95% of AD cases. ApoE4 disrupts memory function in rodents. Further studies have indicated that fragments of apoE may contribute to both plaque and tangle formation. Thus, the epidemiologic and basic science evidence suggest that apoE genotype accounts for the vast majority of AD risk and pathology.</abstract><cop>London</cop><pub>Elsevier Inc</pub><pmid>15172743</pmid><doi>10.1016/j.neurobiolaging.2003.12.023</doi><tpages>10</tpages></addata></record> |
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| subjects | AD pathology AD risk Age Factors Alzheimer Disease - epidemiology Alzheimer Disease - etiology Alzheimer Disease - genetics Animals ApoE genotype Apolipoproteins E - classification Apolipoproteins E - genetics Apolipoproteins E - metabolism Biological and medical sciences Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Disease Models, Animal Gene Frequency Genetic Predisposition to Disease Genotype Humans Medical sciences Memory Disorders - etiology Memory Disorders - genetics Neurofibrillary Tangles - genetics Neurology Plaque, Amyloid - genetics Risk Sex Factors |
| title | ApoE genotype accounts for the vast majority of AD risk and AD pathology |
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