Developmental and vascular risk factors for Alzheimer's disease
To investigate developmental and vascular risk factors for Alzheimer's disease (AD), we examined 90 incident cases of probable AD in a cohort of 1859 individuals followed prospectively for six years. The presence of the APOE-ɛ4 allele was the strongest risk factor, and with increasing survival...
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| Veröffentlicht in: | Neurobiology of aging 2005-03, Vol.26 (3), p.325-334 |
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| creator | Borenstein, Amy R. Wu, Yougui Mortimer, James A. Schellenberg, Gerard D. McCormick, Wayne C. Bowen, James D. McCurry, Susan Larson, Eric B. |
| description | To investigate developmental and vascular risk factors for Alzheimer's disease (AD), we examined 90 incident cases of probable AD in a cohort of 1859 individuals followed prospectively for six years. The presence of the APOE-ɛ4 allele was the strongest risk factor, and with increasing survival age, the effect of ɛ4 diminished. Among ɛ4 positives, developmental risk factors such as smaller head circumference (≤54.4
cm) and having more than four children in the household at age 2–3 were independently associated with incident AD (hazard ratio (HR)
=
2.6 (95% CI 1.04–6.3) and 3.3 (1.2–9.2), respectively). Among ɛ4 negatives, vascular risk factors were related to AD risk (self-reported diagnoses of transient ischemic attack and diabetes (HR
=
5.1, 95% CI 1.7–15.5; HR 3.3, 95% CI 1.4–8.1)). These findings indicate that clinical AD is a result of early life as well as later life risk factors, and that genetic predisposition to the disease may modify the constellation of predictors. |
| doi_str_mv | 10.1016/j.neurobiolaging.2004.04.010 |
| format | Article |
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cm) and having more than four children in the household at age 2–3 were independently associated with incident AD (hazard ratio (HR)
=
2.6 (95% CI 1.04–6.3) and 3.3 (1.2–9.2), respectively). Among ɛ4 negatives, vascular risk factors were related to AD risk (self-reported diagnoses of transient ischemic attack and diabetes (HR
=
5.1, 95% CI 1.7–15.5; HR 3.3, 95% CI 1.4–8.1)). These findings indicate that clinical AD is a result of early life as well as later life risk factors, and that genetic predisposition to the disease may modify the constellation of predictors.</description><identifier>ISSN: 0197-4580</identifier><identifier>EISSN: 1558-1497</identifier><identifier>DOI: 10.1016/j.neurobiolaging.2004.04.010</identifier><identifier>PMID: 15639310</identifier><identifier>CODEN: NEAGDO</identifier><language>eng</language><publisher>London: Elsevier Inc</publisher><subject>Age Factors ; Aged ; Aged, 80 and over ; Alzheimer Disease - ethnology ; Alzheimer Disease - genetics ; Alzheimer Disease - pathology ; Alzheimer's disease ; Apolipoprotein E ; Apolipoprotein E4 ; Apolipoproteins E - genetics ; Asian Americans - genetics ; Biological and medical sciences ; Blood Pressure ; Brain - pathology ; Brain reserve capacity ; Cardiovascular Diseases - ethnology ; Cohort Studies ; Comorbidity ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Developmental ; Diabetes Mellitus - ethnology ; Educational Status ; Female ; Gene Frequency - genetics ; Humans ; Hypertension - ethnology ; Japan - ethnology ; Male ; Medical sciences ; Neurology ; Organ Size ; Prospective Studies ; Risk Factors ; Siblings ; Socioeconomic Factors ; Vascular ; Washington - epidemiology</subject><ispartof>Neurobiology of aging, 2005-03, Vol.26 (3), p.325-334</ispartof><rights>2004 Elsevier Inc.</rights><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c414t-467e3ef581f339f0d335e218a6df514f10c3e2db16df01c29a8d04dc20a32b863</citedby><cites>FETCH-LOGICAL-c414t-467e3ef581f339f0d335e218a6df514f10c3e2db16df01c29a8d04dc20a32b863</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.2004.04.010$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>309,310,314,780,784,789,790,3550,23930,23931,25140,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16411135$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15639310$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Borenstein, Amy R.</creatorcontrib><creatorcontrib>Wu, Yougui</creatorcontrib><creatorcontrib>Mortimer, James A.</creatorcontrib><creatorcontrib>Schellenberg, Gerard D.</creatorcontrib><creatorcontrib>McCormick, Wayne C.</creatorcontrib><creatorcontrib>Bowen, James D.</creatorcontrib><creatorcontrib>McCurry, Susan</creatorcontrib><creatorcontrib>Larson, Eric B.</creatorcontrib><title>Developmental and vascular risk factors for Alzheimer's disease</title><title>Neurobiology of aging</title><addtitle>Neurobiol Aging</addtitle><description>To investigate developmental and vascular risk factors for Alzheimer's disease (AD), we examined 90 incident cases of probable AD in a cohort of 1859 individuals followed prospectively for six years. The presence of the APOE-ɛ4 allele was the strongest risk factor, and with increasing survival age, the effect of ɛ4 diminished. Among ɛ4 positives, developmental risk factors such as smaller head circumference (≤54.4
cm) and having more than four children in the household at age 2–3 were independently associated with incident AD (hazard ratio (HR)
=
2.6 (95% CI 1.04–6.3) and 3.3 (1.2–9.2), respectively). Among ɛ4 negatives, vascular risk factors were related to AD risk (self-reported diagnoses of transient ischemic attack and diabetes (HR
=
5.1, 95% CI 1.7–15.5; HR 3.3, 95% CI 1.4–8.1)). These findings indicate that clinical AD is a result of early life as well as later life risk factors, and that genetic predisposition to the disease may modify the constellation of predictors.</description><subject>Age Factors</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Alzheimer Disease - ethnology</subject><subject>Alzheimer Disease - genetics</subject><subject>Alzheimer Disease - pathology</subject><subject>Alzheimer's disease</subject><subject>Apolipoprotein E</subject><subject>Apolipoprotein E4</subject><subject>Apolipoproteins E - genetics</subject><subject>Asian Americans - genetics</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure</subject><subject>Brain - pathology</subject><subject>Brain reserve capacity</subject><subject>Cardiovascular Diseases - ethnology</subject><subject>Cohort Studies</subject><subject>Comorbidity</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Developmental</subject><subject>Diabetes Mellitus - ethnology</subject><subject>Educational Status</subject><subject>Female</subject><subject>Gene Frequency - genetics</subject><subject>Humans</subject><subject>Hypertension - ethnology</subject><subject>Japan - ethnology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Neurology</subject><subject>Organ Size</subject><subject>Prospective Studies</subject><subject>Risk Factors</subject><subject>Siblings</subject><subject>Socioeconomic Factors</subject><subject>Vascular</subject><subject>Washington - epidemiology</subject><issn>0197-4580</issn><issn>1558-1497</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkN9LHDEQx4O06NX6L8g-WPu058wm2R9QELG1FQRf2ueQSyY21-zmTHYP9K_vHncgfSsMDAOf78zwYewCYYmA9dV6OdCU4srHoJ_88LSsAMRyVwhHbIFStiWKrnnHFoBdUwrZwgn7kPMaABrR1MfsBGXNO46wYNdfaUshbnoaRh0KPdhiq7OZgk5F8vlP4bQZY8qFi6m4Ca-_yfeUPufC-kw600f23umQ6ezQT9mvu28_b3-UD4_f729vHkojUIylqBvi5GSLjvPOgeVcUoWtrq2TKByC4VTZFc4zoKk63VoQ1lSgebVqa37KLvd7Nyk-T5RH1ftsKAQ9UJyyqhsuW87FDH7ZgybFnBM5tUm-1-lFIaidQLVW_wpUO4FqVwhz_PxwZ1r1ZN_CB2Mz8OkAzJp0cEkPxuc3rhaIyOXM3e05mq1sPSWVjafBkPWJzKhs9P_30V9UfJcr</recordid><startdate>20050301</startdate><enddate>20050301</enddate><creator>Borenstein, Amy R.</creator><creator>Wu, Yougui</creator><creator>Mortimer, James A.</creator><creator>Schellenberg, Gerard D.</creator><creator>McCormick, Wayne C.</creator><creator>Bowen, James D.</creator><creator>McCurry, Susan</creator><creator>Larson, Eric B.</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>7X8</scope></search><sort><creationdate>20050301</creationdate><title>Developmental and vascular risk factors for Alzheimer's disease</title><author>Borenstein, Amy R. ; Wu, Yougui ; Mortimer, James A. ; Schellenberg, Gerard D. ; McCormick, Wayne C. ; Bowen, James D. ; McCurry, Susan ; Larson, Eric B.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c414t-467e3ef581f339f0d335e218a6df514f10c3e2db16df01c29a8d04dc20a32b863</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Age Factors</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Alzheimer Disease - ethnology</topic><topic>Alzheimer Disease - genetics</topic><topic>Alzheimer Disease - pathology</topic><topic>Alzheimer's disease</topic><topic>Apolipoprotein E</topic><topic>Apolipoprotein E4</topic><topic>Apolipoproteins E - genetics</topic><topic>Asian Americans - genetics</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure</topic><topic>Brain - pathology</topic><topic>Brain reserve capacity</topic><topic>Cardiovascular Diseases - ethnology</topic><topic>Cohort Studies</topic><topic>Comorbidity</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Developmental</topic><topic>Diabetes Mellitus - ethnology</topic><topic>Educational Status</topic><topic>Female</topic><topic>Gene Frequency - genetics</topic><topic>Humans</topic><topic>Hypertension - ethnology</topic><topic>Japan - ethnology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Neurology</topic><topic>Organ Size</topic><topic>Prospective Studies</topic><topic>Risk Factors</topic><topic>Siblings</topic><topic>Socioeconomic Factors</topic><topic>Vascular</topic><topic>Washington - epidemiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Borenstein, Amy R.</creatorcontrib><creatorcontrib>Wu, Yougui</creatorcontrib><creatorcontrib>Mortimer, James A.</creatorcontrib><creatorcontrib>Schellenberg, Gerard D.</creatorcontrib><creatorcontrib>McCormick, Wayne C.</creatorcontrib><creatorcontrib>Bowen, James D.</creatorcontrib><creatorcontrib>McCurry, Susan</creatorcontrib><creatorcontrib>Larson, Eric B.</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>MEDLINE - Academic</collection><jtitle>Neurobiology of aging</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Borenstein, Amy R.</au><au>Wu, Yougui</au><au>Mortimer, James A.</au><au>Schellenberg, Gerard D.</au><au>McCormick, Wayne C.</au><au>Bowen, James D.</au><au>McCurry, Susan</au><au>Larson, Eric B.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Developmental and vascular risk factors for Alzheimer's disease</atitle><jtitle>Neurobiology of aging</jtitle><addtitle>Neurobiol Aging</addtitle><date>2005-03-01</date><risdate>2005</risdate><volume>26</volume><issue>3</issue><spage>325</spage><epage>334</epage><pages>325-334</pages><issn>0197-4580</issn><eissn>1558-1497</eissn><coden>NEAGDO</coden><abstract>To investigate developmental and vascular risk factors for Alzheimer's disease (AD), we examined 90 incident cases of probable AD in a cohort of 1859 individuals followed prospectively for six years. The presence of the APOE-ɛ4 allele was the strongest risk factor, and with increasing survival age, the effect of ɛ4 diminished. Among ɛ4 positives, developmental risk factors such as smaller head circumference (≤54.4
cm) and having more than four children in the household at age 2–3 were independently associated with incident AD (hazard ratio (HR)
=
2.6 (95% CI 1.04–6.3) and 3.3 (1.2–9.2), respectively). Among ɛ4 negatives, vascular risk factors were related to AD risk (self-reported diagnoses of transient ischemic attack and diabetes (HR
=
5.1, 95% CI 1.7–15.5; HR 3.3, 95% CI 1.4–8.1)). These findings indicate that clinical AD is a result of early life as well as later life risk factors, and that genetic predisposition to the disease may modify the constellation of predictors.</abstract><cop>London</cop><pub>Elsevier Inc</pub><pmid>15639310</pmid><doi>10.1016/j.neurobiolaging.2004.04.010</doi><tpages>10</tpages></addata></record> |
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| subjects | Age Factors Aged Aged, 80 and over Alzheimer Disease - ethnology Alzheimer Disease - genetics Alzheimer Disease - pathology Alzheimer's disease Apolipoprotein E Apolipoprotein E4 Apolipoproteins E - genetics Asian Americans - genetics Biological and medical sciences Blood Pressure Brain - pathology Brain reserve capacity Cardiovascular Diseases - ethnology Cohort Studies Comorbidity Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Developmental Diabetes Mellitus - ethnology Educational Status Female Gene Frequency - genetics Humans Hypertension - ethnology Japan - ethnology Male Medical sciences Neurology Organ Size Prospective Studies Risk Factors Siblings Socioeconomic Factors Vascular Washington - epidemiology |
| title | Developmental and vascular risk factors for Alzheimer's disease |
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