Age and apoE associations with complex pathologic features in Alzheimer's disease
Abstract The risk for Alzheimer's disease (AD) is influenced by both age and ApoE status. The present study addresses the associations of age and ApoE status on complex pathologic features in AD ( n = 81) including coexistent cerebrovascular disease (CVD), argyrophilic grain disease (AGD), and...
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| Veröffentlicht in: | Journal of the neurological sciences 2008-10, Vol.273 (1), p.34-39 |
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| container_title | Journal of the neurological sciences |
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| creator | Jicha, Gregory A Parisi, Joseph E Dickson, Dennis W Cha, Ruth H Johnson, Kris A Smith, Glenn E Boeve, Bradley F Petersen, Ronald C Knopman, David S |
| description | Abstract The risk for Alzheimer's disease (AD) is influenced by both age and ApoE status. The present study addresses the associations of age and ApoE status on complex pathologic features in AD ( n = 81) including coexistent cerebrovascular disease (CVD), argyrophilic grain disease (AGD), and Lewy body disease (LBD). The frequency of coexistent cerebrovascular disease increased with increasing age. Age and ApoE status were differentially associated with atherosclerosis, lacunar infarctions, and microvascular pathology. Coexistent Lewy body pathology was negatively associated with age, dropping off abruptly after age 90. The presence of an ApoE ε4 allele was associated with an increased frequency of coexistent LBD. Logistic regression analyses demonstrated both dependent and independent effects of age and ApoE status on the presence of coexistent Lewy body pathology in AD. While the decreasing frequency of LBD in AD after age 90 could be partly accounted for by a lower probability of an ApoE ε4 allele, the independent association with age suggests either 1) a survival effect, 2) decreased incidence with advancing age, or 3) both. |
| doi_str_mv | 10.1016/j.jns.2008.06.008 |
| format | Article |
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The present study addresses the associations of age and ApoE status on complex pathologic features in AD ( n = 81) including coexistent cerebrovascular disease (CVD), argyrophilic grain disease (AGD), and Lewy body disease (LBD). The frequency of coexistent cerebrovascular disease increased with increasing age. Age and ApoE status were differentially associated with atherosclerosis, lacunar infarctions, and microvascular pathology. Coexistent Lewy body pathology was negatively associated with age, dropping off abruptly after age 90. The presence of an ApoE ε4 allele was associated with an increased frequency of coexistent LBD. Logistic regression analyses demonstrated both dependent and independent effects of age and ApoE status on the presence of coexistent Lewy body pathology in AD. While the decreasing frequency of LBD in AD after age 90 could be partly accounted for by a lower probability of an ApoE ε4 allele, the independent association with age suggests either 1) a survival effect, 2) decreased incidence with advancing age, or 3) both.</description><identifier>ISSN: 0022-510X</identifier><identifier>EISSN: 1878-5883</identifier><identifier>DOI: 10.1016/j.jns.2008.06.008</identifier><identifier>PMID: 18653200</identifier><identifier>CODEN: JNSCAG</identifier><language>eng</language><publisher>Shannon: Elsevier B.V</publisher><subject>age ; Age Factors ; Aged ; Aged, 80 and over ; Aging ; Alzheimer Disease - complications ; Alzheimer Disease - genetics ; Alzheimer Disease - mortality ; Alzheimer Disease - pathology ; Alzheimer's disease ; Apolipoprotein E ; Apolipoprotein E4 - genetics ; Argyrophilic grains ; Biological and medical sciences ; Cerebral Amyloid Angiopathy - complications ; Cerebral Amyloid Angiopathy - genetics ; Cerebrovascular disease ; Cerebrovascular Disorders - complications ; Cerebrovascular Disorders - genetics ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Female ; Humans ; Lewy body disease ; Lewy Body Disease - complications ; Lewy Body Disease - genetics ; Lewy Body Disease - mortality ; Lewy Body Disease - pathology ; Logistic Models ; Male ; Medical sciences ; Neurology ; Retrospective Studies</subject><ispartof>Journal of the neurological sciences, 2008-10, Vol.273 (1), p.34-39</ispartof><rights>Elsevier B.V.</rights><rights>2008 Elsevier B.V.</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c565t-e6ce345fd2be7efc427c2d5b774ed336e2d58a42f9772fe9315bc480e84e15d53</citedby><cites>FETCH-LOGICAL-c565t-e6ce345fd2be7efc427c2d5b774ed336e2d58a42f9772fe9315bc480e84e15d53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jns.2008.06.008$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,778,782,883,3539,27911,27912,45982</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20680448$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18653200$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jicha, Gregory A</creatorcontrib><creatorcontrib>Parisi, Joseph E</creatorcontrib><creatorcontrib>Dickson, Dennis W</creatorcontrib><creatorcontrib>Cha, Ruth H</creatorcontrib><creatorcontrib>Johnson, Kris A</creatorcontrib><creatorcontrib>Smith, Glenn E</creatorcontrib><creatorcontrib>Boeve, Bradley F</creatorcontrib><creatorcontrib>Petersen, Ronald C</creatorcontrib><creatorcontrib>Knopman, David S</creatorcontrib><title>Age and apoE associations with complex pathologic features in Alzheimer's disease</title><title>Journal of the neurological sciences</title><addtitle>J Neurol Sci</addtitle><description>Abstract The risk for Alzheimer's disease (AD) is influenced by both age and ApoE status. The present study addresses the associations of age and ApoE status on complex pathologic features in AD ( n = 81) including coexistent cerebrovascular disease (CVD), argyrophilic grain disease (AGD), and Lewy body disease (LBD). The frequency of coexistent cerebrovascular disease increased with increasing age. Age and ApoE status were differentially associated with atherosclerosis, lacunar infarctions, and microvascular pathology. Coexistent Lewy body pathology was negatively associated with age, dropping off abruptly after age 90. The presence of an ApoE ε4 allele was associated with an increased frequency of coexistent LBD. Logistic regression analyses demonstrated both dependent and independent effects of age and ApoE status on the presence of coexistent Lewy body pathology in AD. While the decreasing frequency of LBD in AD after age 90 could be partly accounted for by a lower probability of an ApoE ε4 allele, the independent association with age suggests either 1) a survival effect, 2) decreased incidence with advancing age, or 3) both.</description><subject>age</subject><subject>Age Factors</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Aging</subject><subject>Alzheimer Disease - complications</subject><subject>Alzheimer Disease - genetics</subject><subject>Alzheimer Disease - mortality</subject><subject>Alzheimer Disease - pathology</subject><subject>Alzheimer's disease</subject><subject>Apolipoprotein E</subject><subject>Apolipoprotein E4 - genetics</subject><subject>Argyrophilic grains</subject><subject>Biological and medical sciences</subject><subject>Cerebral Amyloid Angiopathy - complications</subject><subject>Cerebral Amyloid Angiopathy - genetics</subject><subject>Cerebrovascular disease</subject><subject>Cerebrovascular Disorders - complications</subject><subject>Cerebrovascular Disorders - genetics</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Female</subject><subject>Humans</subject><subject>Lewy body disease</subject><subject>Lewy Body Disease - complications</subject><subject>Lewy Body Disease - genetics</subject><subject>Lewy Body Disease - mortality</subject><subject>Lewy Body Disease - pathology</subject><subject>Logistic Models</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Neurology</subject><subject>Retrospective Studies</subject><issn>0022-510X</issn><issn>1878-5883</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkl-L1DAUxYso7rj6AXyRvKhPrUnapCnCwrCsq7AgooJvIZPezqS2yZjbrq6fflNmWP886NNNyO-c3OTcLHvKaMEok6_6ovdYcEpVQWWRyr1sxVStcqFUeT9bUcp5Lhj9cpI9QuwppVKp5mF2wpQUZdKtsg_rLRDjW2L24YIYxGCdmVzwSL67aUdsGPcD_CB7M-3CELbOkg7MNEdA4jxZDz934EaIL5G0DsEgPM4edGZAeHKsp9nnNxefzt_mV-8v352vr3IrpJhykBbKSnQt30ANna14bXkrNnVdQVuWEtJGmYp3TV3zDpqSiY2tFAVVAROtKE-zs4Pvft6M0FrwUzSD3kc3mnijg3H6zxPvdnobrjUXslG8TAYvjgYxfJsBJz06tDAMxkOYUcumUrwS_L8gS2DDFEsgO4A2BsQI3V03jOolMd3rlJheEtNU6lSS5tnvz_ilOEaUgOdHwKA1QxeNtw7vOJ4ypVW1GL0-cJA-_dpB1GgdeAuti2An3Qb3zzbO_lLbwXmXLvwKN4B9mKNPaWqmkWuqPy6jtUwWVWlVl7K8BVEpyjs</recordid><startdate>20081015</startdate><enddate>20081015</enddate><creator>Jicha, Gregory A</creator><creator>Parisi, Joseph E</creator><creator>Dickson, Dennis W</creator><creator>Cha, Ruth H</creator><creator>Johnson, Kris A</creator><creator>Smith, Glenn E</creator><creator>Boeve, Bradley F</creator><creator>Petersen, Ronald C</creator><creator>Knopman, David S</creator><general>Elsevier B.V</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><scope>5PM</scope></search><sort><creationdate>20081015</creationdate><title>Age and apoE associations with complex pathologic features in Alzheimer's disease</title><author>Jicha, Gregory A ; Parisi, Joseph E ; Dickson, Dennis W ; Cha, Ruth H ; Johnson, Kris A ; Smith, Glenn E ; Boeve, Bradley F ; Petersen, Ronald C ; Knopman, David S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c565t-e6ce345fd2be7efc427c2d5b774ed336e2d58a42f9772fe9315bc480e84e15d53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>age</topic><topic>Age Factors</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Aging</topic><topic>Alzheimer Disease - complications</topic><topic>Alzheimer Disease - genetics</topic><topic>Alzheimer Disease - mortality</topic><topic>Alzheimer Disease - pathology</topic><topic>Alzheimer's disease</topic><topic>Apolipoprotein E</topic><topic>Apolipoprotein E4 - genetics</topic><topic>Argyrophilic grains</topic><topic>Biological and medical sciences</topic><topic>Cerebral Amyloid Angiopathy - complications</topic><topic>Cerebral Amyloid Angiopathy - genetics</topic><topic>Cerebrovascular disease</topic><topic>Cerebrovascular Disorders - complications</topic><topic>Cerebrovascular Disorders - genetics</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Female</topic><topic>Humans</topic><topic>Lewy body disease</topic><topic>Lewy Body Disease - complications</topic><topic>Lewy Body Disease - genetics</topic><topic>Lewy Body Disease - mortality</topic><topic>Lewy Body Disease - pathology</topic><topic>Logistic Models</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Neurology</topic><topic>Retrospective Studies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jicha, Gregory A</creatorcontrib><creatorcontrib>Parisi, Joseph E</creatorcontrib><creatorcontrib>Dickson, Dennis W</creatorcontrib><creatorcontrib>Cha, Ruth H</creatorcontrib><creatorcontrib>Johnson, Kris A</creatorcontrib><creatorcontrib>Smith, Glenn E</creatorcontrib><creatorcontrib>Boeve, Bradley F</creatorcontrib><creatorcontrib>Petersen, Ronald C</creatorcontrib><creatorcontrib>Knopman, David S</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of the neurological sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jicha, Gregory A</au><au>Parisi, Joseph E</au><au>Dickson, Dennis W</au><au>Cha, Ruth H</au><au>Johnson, Kris A</au><au>Smith, Glenn E</au><au>Boeve, Bradley F</au><au>Petersen, Ronald C</au><au>Knopman, David S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Age and apoE associations with complex pathologic features in Alzheimer's disease</atitle><jtitle>Journal of the neurological sciences</jtitle><addtitle>J Neurol Sci</addtitle><date>2008-10-15</date><risdate>2008</risdate><volume>273</volume><issue>1</issue><spage>34</spage><epage>39</epage><pages>34-39</pages><issn>0022-510X</issn><eissn>1878-5883</eissn><coden>JNSCAG</coden><abstract>Abstract The risk for Alzheimer's disease (AD) is influenced by both age and ApoE status. The present study addresses the associations of age and ApoE status on complex pathologic features in AD ( n = 81) including coexistent cerebrovascular disease (CVD), argyrophilic grain disease (AGD), and Lewy body disease (LBD). The frequency of coexistent cerebrovascular disease increased with increasing age. Age and ApoE status were differentially associated with atherosclerosis, lacunar infarctions, and microvascular pathology. Coexistent Lewy body pathology was negatively associated with age, dropping off abruptly after age 90. The presence of an ApoE ε4 allele was associated with an increased frequency of coexistent LBD. Logistic regression analyses demonstrated both dependent and independent effects of age and ApoE status on the presence of coexistent Lewy body pathology in AD. While the decreasing frequency of LBD in AD after age 90 could be partly accounted for by a lower probability of an ApoE ε4 allele, the independent association with age suggests either 1) a survival effect, 2) decreased incidence with advancing age, or 3) both.</abstract><cop>Shannon</cop><pub>Elsevier B.V</pub><pmid>18653200</pmid><doi>10.1016/j.jns.2008.06.008</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | age Age Factors Aged Aged, 80 and over Aging Alzheimer Disease - complications Alzheimer Disease - genetics Alzheimer Disease - mortality Alzheimer Disease - pathology Alzheimer's disease Apolipoprotein E Apolipoprotein E4 - genetics Argyrophilic grains Biological and medical sciences Cerebral Amyloid Angiopathy - complications Cerebral Amyloid Angiopathy - genetics Cerebrovascular disease Cerebrovascular Disorders - complications Cerebrovascular Disorders - genetics Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Female Humans Lewy body disease Lewy Body Disease - complications Lewy Body Disease - genetics Lewy Body Disease - mortality Lewy Body Disease - pathology Logistic Models Male Medical sciences Neurology Retrospective Studies |
| title | Age and apoE associations with complex pathologic features in Alzheimer's disease |
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