Two Types of Sporadic Cerebral Amyloid Angiopathy
Cerebral amyloid angiopathy (CAA) is a type of β-amyloidosis that occurs in leptomeningeal and cortical vessels of the elderly. In a sample of 41 CAA cases including 16 Alzheimer disease (AD) cases and 28 controls, we show that 2 types of sporadic CAA existThe first type is characterized by immunohi...
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| Veröffentlicht in: | Journal of neuropathology and experimental neurology 2002-03, Vol.61 (3), p.282-293 |
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| creator | THAL, DIETMAR RUDOLF GHEBREMEDHIN, ESTIFANOS RÜB, UDO YAMAGUCHI, HARUYASU TREDICI, KELLY DEL BRAAK, HEIKO |
| description | Cerebral amyloid angiopathy (CAA) is a type of β-amyloidosis that occurs in leptomeningeal and cortical vessels of the elderly. In a sample of 41 CAA cases including 16 Alzheimer disease (AD) cases and 28 controls, we show that 2 types of sporadic CAA existThe first type is characterized by immunohistochemically detectable amyloid β-protein (Aβ) in cortical capillaries, leptomeningeal and cortical arteries, arterioles, veins, and venules. It is referred to here as CAA-Type 1. The second type of CAA also exhibits immunohistochemically detectable Aβ deposits in leptomeningeal and cortical vessels, with the exception of cortical capillaries. This type is termed CAA-Type 2. In cases with CAA-Type 1, the frequency of the apolipoprotein E (ApoE) 4 allele is more than 4 times greater than in CAA-Type 2 cases and in controls. CAA-Type 2 cases have a higher 2 allele frequency than CAA-Type 1 cases and controls. The ratio of CAA-Type 2 to CAA-Type 1 cases does not shift significantly with respect to the severity of AD-related β-amyloidosis, with respect to degrees of CAA-severity, or with increasing age. Therefore, CAA-Type 1 is unlikely to be the late stage of CAA-Type 2; rather, they represent 2 different entities. Since both the ApoE 2 and the 4 allele are known to be risk factors for CAA, we can assign the risk factor ApoE 4 to a distinct morphological type of CAA. The ApoE 4 allele constitutes a risk factor for CAA-Type 1 and, as such, for neuropil-associated dyshoric vascular Aβ deposition in capillaries, whereas the 2 allele does not. CAA-Type 2 is not associated with the 4 allele as a risk factor but shows a higher 2 allele frequency than CAA-Type 1 cases and controls in our sample. |
| doi_str_mv | 10.1093/jnen/61.3.282 |
| format | Article |
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In a sample of 41 CAA cases including 16 Alzheimer disease (AD) cases and 28 controls, we show that 2 types of sporadic CAA existThe first type is characterized by immunohistochemically detectable amyloid β-protein (Aβ) in cortical capillaries, leptomeningeal and cortical arteries, arterioles, veins, and venules. It is referred to here as CAA-Type 1. The second type of CAA also exhibits immunohistochemically detectable Aβ deposits in leptomeningeal and cortical vessels, with the exception of cortical capillaries. This type is termed CAA-Type 2. In cases with CAA-Type 1, the frequency of the apolipoprotein E (ApoE) 4 allele is more than 4 times greater than in CAA-Type 2 cases and in controls. CAA-Type 2 cases have a higher 2 allele frequency than CAA-Type 1 cases and controls. The ratio of CAA-Type 2 to CAA-Type 1 cases does not shift significantly with respect to the severity of AD-related β-amyloidosis, with respect to degrees of CAA-severity, or with increasing age. Therefore, CAA-Type 1 is unlikely to be the late stage of CAA-Type 2; rather, they represent 2 different entities. Since both the ApoE 2 and the 4 allele are known to be risk factors for CAA, we can assign the risk factor ApoE 4 to a distinct morphological type of CAA. The ApoE 4 allele constitutes a risk factor for CAA-Type 1 and, as such, for neuropil-associated dyshoric vascular Aβ deposition in capillaries, whereas the 2 allele does not. CAA-Type 2 is not associated with the 4 allele as a risk factor but shows a higher 2 allele frequency than CAA-Type 1 cases and controls in our sample.</description><identifier>ISSN: 0022-3069</identifier><identifier>EISSN: 1554-6578</identifier><identifier>DOI: 10.1093/jnen/61.3.282</identifier><identifier>PMID: 11895043</identifier><identifier>CODEN: JNENAD</identifier><language>eng</language><publisher>Hagerstown, MD: American Association of Neuropathologists, Inc</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Aging - physiology ; Alleles ; Alzheimer Disease - complications ; Amyloid beta-Peptides - metabolism ; Amyloidosis - complications ; Apolipoproteins E - genetics ; Biological and medical sciences ; Blood Vessels - metabolism ; Brain Diseases - complications ; Capillaries - metabolism ; Cerebral Amyloid Angiopathy - classification ; Cerebral Amyloid Angiopathy - complications ; Cerebral Amyloid Angiopathy - genetics ; Cerebral Amyloid Angiopathy - physiopathology ; Cerebral Infarction - complications ; Cerebrovascular Circulation ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Female ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Humans ; Male ; Medical sciences ; Middle Aged ; Neurology ; Reference Values ; Severity of Illness Index</subject><ispartof>Journal of neuropathology and experimental neurology, 2002-03, Vol.61 (3), p.282-293</ispartof><rights>2002 American Association of Neuropathologists, Inc</rights><rights>2002 INIST-CNRS</rights><rights>Copyright American Association of Neuropathologists, Inc. Mar 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5271-e43caf6e747b84688f18b322433d4b33a73f2bc4335c55fb4367b56ce067dc473</citedby><cites>FETCH-LOGICAL-c5271-e43caf6e747b84688f18b322433d4b33a73f2bc4335c55fb4367b56ce067dc473</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13546933$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11895043$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>THAL, DIETMAR RUDOLF</creatorcontrib><creatorcontrib>GHEBREMEDHIN, ESTIFANOS</creatorcontrib><creatorcontrib>RÜB, UDO</creatorcontrib><creatorcontrib>YAMAGUCHI, HARUYASU</creatorcontrib><creatorcontrib>TREDICI, KELLY DEL</creatorcontrib><creatorcontrib>BRAAK, HEIKO</creatorcontrib><title>Two Types of Sporadic Cerebral Amyloid Angiopathy</title><title>Journal of neuropathology and experimental neurology</title><addtitle>J Neuropathol Exp Neurol</addtitle><description>Cerebral amyloid angiopathy (CAA) is a type of β-amyloidosis that occurs in leptomeningeal and cortical vessels of the elderly. In a sample of 41 CAA cases including 16 Alzheimer disease (AD) cases and 28 controls, we show that 2 types of sporadic CAA existThe first type is characterized by immunohistochemically detectable amyloid β-protein (Aβ) in cortical capillaries, leptomeningeal and cortical arteries, arterioles, veins, and venules. It is referred to here as CAA-Type 1. The second type of CAA also exhibits immunohistochemically detectable Aβ deposits in leptomeningeal and cortical vessels, with the exception of cortical capillaries. This type is termed CAA-Type 2. In cases with CAA-Type 1, the frequency of the apolipoprotein E (ApoE) 4 allele is more than 4 times greater than in CAA-Type 2 cases and in controls. CAA-Type 2 cases have a higher 2 allele frequency than CAA-Type 1 cases and controls. The ratio of CAA-Type 2 to CAA-Type 1 cases does not shift significantly with respect to the severity of AD-related β-amyloidosis, with respect to degrees of CAA-severity, or with increasing age. Therefore, CAA-Type 1 is unlikely to be the late stage of CAA-Type 2; rather, they represent 2 different entities. Since both the ApoE 2 and the 4 allele are known to be risk factors for CAA, we can assign the risk factor ApoE 4 to a distinct morphological type of CAA. The ApoE 4 allele constitutes a risk factor for CAA-Type 1 and, as such, for neuropil-associated dyshoric vascular Aβ deposition in capillaries, whereas the 2 allele does not. CAA-Type 2 is not associated with the 4 allele as a risk factor but shows a higher 2 allele frequency than CAA-Type 1 cases and controls in our sample.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Aging - physiology</subject><subject>Alleles</subject><subject>Alzheimer Disease - complications</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>Amyloidosis - complications</subject><subject>Apolipoproteins E - genetics</subject><subject>Biological and medical sciences</subject><subject>Blood Vessels - metabolism</subject><subject>Brain Diseases - complications</subject><subject>Capillaries - metabolism</subject><subject>Cerebral Amyloid Angiopathy - classification</subject><subject>Cerebral Amyloid Angiopathy - complications</subject><subject>Cerebral Amyloid Angiopathy - genetics</subject><subject>Cerebral Amyloid Angiopathy - physiopathology</subject><subject>Cerebral Infarction - complications</subject><subject>Cerebrovascular Circulation</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Female</subject><subject>Gene Frequency</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Neurology</subject><subject>Reference Values</subject><subject>Severity of Illness Index</subject><issn>0022-3069</issn><issn>1554-6578</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqF0U2L2zAQBmBRunTTbY-9FlNob85qNPo8htDdFhZ6aHoWsiw3Th3LlWJC_v0qJLDQSw_DMPAwMO8Q8gHoEqjB-90YxnsJS1wyzV6RBQjBaymUfk0WlDJWI5XmlrzNeUcpNdTwN-QWQBtBOS4IbI6x2pymkKvYVT-nmFzb-2odUmiSG6rV_jTEvq1W4-8-Tu6wPb0jN50bcnh_7Xfk18PXzfpb_fTj8ft69VR7wRTUgaN3nQyKq0ZzqXUHukHGOGLLG0SnsGONL6PwQnQNR6kaIX2gUrWeK7wjXy57pxT_ziEf7L7PPgyDG0Ocs1UgGHAq_wvBcNBUnOGnf-AuzmksR1jGjFQgjS6oviCfYs4pdHZK_d6lkwVqz4nbc-JWgkVbEi_-43Xp3OxD-6KvERfw-Qpc9m7okht9n18cCi4Nnh2_uGMcDiHlP8N8DMlugxsOW1t-RwVVrGblqRTLVJcCwGdT3ZXb</recordid><startdate>200203</startdate><enddate>200203</enddate><creator>THAL, DIETMAR RUDOLF</creator><creator>GHEBREMEDHIN, ESTIFANOS</creator><creator>RÜB, UDO</creator><creator>YAMAGUCHI, HARUYASU</creator><creator>TREDICI, KELLY DEL</creator><creator>BRAAK, HEIKO</creator><general>American Association of Neuropathologists, Inc</general><general>Lippincott Williams & Wilkins</general><general>Oxford University Press</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AF</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>200203</creationdate><title>Two Types of Sporadic Cerebral Amyloid Angiopathy</title><author>THAL, DIETMAR RUDOLF ; GHEBREMEDHIN, ESTIFANOS ; RÜB, UDO ; YAMAGUCHI, HARUYASU ; TREDICI, KELLY DEL ; BRAAK, HEIKO</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5271-e43caf6e747b84688f18b322433d4b33a73f2bc4335c55fb4367b56ce067dc473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Aging - physiology</topic><topic>Alleles</topic><topic>Alzheimer Disease - complications</topic><topic>Amyloid beta-Peptides - metabolism</topic><topic>Amyloidosis - complications</topic><topic>Apolipoproteins E - genetics</topic><topic>Biological and medical sciences</topic><topic>Blood Vessels - metabolism</topic><topic>Brain Diseases - complications</topic><topic>Capillaries - metabolism</topic><topic>Cerebral Amyloid Angiopathy - classification</topic><topic>Cerebral Amyloid Angiopathy - complications</topic><topic>Cerebral Amyloid Angiopathy - genetics</topic><topic>Cerebral Amyloid Angiopathy - physiopathology</topic><topic>Cerebral Infarction - complications</topic><topic>Cerebrovascular Circulation</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Female</topic><topic>Gene Frequency</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Neurology</topic><topic>Reference Values</topic><topic>Severity of Illness Index</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>THAL, DIETMAR RUDOLF</creatorcontrib><creatorcontrib>GHEBREMEDHIN, ESTIFANOS</creatorcontrib><creatorcontrib>RÜB, UDO</creatorcontrib><creatorcontrib>YAMAGUCHI, HARUYASU</creatorcontrib><creatorcontrib>TREDICI, KELLY DEL</creatorcontrib><creatorcontrib>BRAAK, HEIKO</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>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>SIRS Editorial</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neuropathology and experimental neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>THAL, DIETMAR RUDOLF</au><au>GHEBREMEDHIN, ESTIFANOS</au><au>RÜB, UDO</au><au>YAMAGUCHI, HARUYASU</au><au>TREDICI, KELLY DEL</au><au>BRAAK, HEIKO</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Two Types of Sporadic Cerebral Amyloid Angiopathy</atitle><jtitle>Journal of neuropathology and experimental neurology</jtitle><addtitle>J Neuropathol Exp Neurol</addtitle><date>2002-03</date><risdate>2002</risdate><volume>61</volume><issue>3</issue><spage>282</spage><epage>293</epage><pages>282-293</pages><issn>0022-3069</issn><eissn>1554-6578</eissn><coden>JNENAD</coden><abstract>Cerebral amyloid angiopathy (CAA) is a type of β-amyloidosis that occurs in leptomeningeal and cortical vessels of the elderly. In a sample of 41 CAA cases including 16 Alzheimer disease (AD) cases and 28 controls, we show that 2 types of sporadic CAA existThe first type is characterized by immunohistochemically detectable amyloid β-protein (Aβ) in cortical capillaries, leptomeningeal and cortical arteries, arterioles, veins, and venules. It is referred to here as CAA-Type 1. The second type of CAA also exhibits immunohistochemically detectable Aβ deposits in leptomeningeal and cortical vessels, with the exception of cortical capillaries. This type is termed CAA-Type 2. In cases with CAA-Type 1, the frequency of the apolipoprotein E (ApoE) 4 allele is more than 4 times greater than in CAA-Type 2 cases and in controls. CAA-Type 2 cases have a higher 2 allele frequency than CAA-Type 1 cases and controls. The ratio of CAA-Type 2 to CAA-Type 1 cases does not shift significantly with respect to the severity of AD-related β-amyloidosis, with respect to degrees of CAA-severity, or with increasing age. Therefore, CAA-Type 1 is unlikely to be the late stage of CAA-Type 2; rather, they represent 2 different entities. Since both the ApoE 2 and the 4 allele are known to be risk factors for CAA, we can assign the risk factor ApoE 4 to a distinct morphological type of CAA. The ApoE 4 allele constitutes a risk factor for CAA-Type 1 and, as such, for neuropil-associated dyshoric vascular Aβ deposition in capillaries, whereas the 2 allele does not. CAA-Type 2 is not associated with the 4 allele as a risk factor but shows a higher 2 allele frequency than CAA-Type 1 cases and controls in our sample.</abstract><cop>Hagerstown, MD</cop><pub>American Association of Neuropathologists, Inc</pub><pmid>11895043</pmid><doi>10.1093/jnen/61.3.282</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Aged, 80 and over Aging - physiology Alleles Alzheimer Disease - complications Amyloid beta-Peptides - metabolism Amyloidosis - complications Apolipoproteins E - genetics Biological and medical sciences Blood Vessels - metabolism Brain Diseases - complications Capillaries - metabolism Cerebral Amyloid Angiopathy - classification Cerebral Amyloid Angiopathy - complications Cerebral Amyloid Angiopathy - genetics Cerebral Amyloid Angiopathy - physiopathology Cerebral Infarction - complications Cerebrovascular Circulation Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Female Gene Frequency Genetic Predisposition to Disease Genotype Humans Male Medical sciences Middle Aged Neurology Reference Values Severity of Illness Index |
| title | Two Types of Sporadic Cerebral Amyloid Angiopathy |
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