Sequence variants of IDE are associated with the extent of β-amyloid deposition in the Alzheimer's disease brain
Insulin degrading enzyme, encoded by IDE, plays a primary role in the degradation of amyloid β-protein (Aβ), the deposition of which in senile plaques is one of the defining hallmarks of Alzheimer's disease (AD). We recently identified haplotypes in a broad linkage disequilibrium (LD) block enc...
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| Veröffentlicht in: | Neurobiology of aging 2005-06, Vol.26 (6), p.795-802 |
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| creator | Blomqvist, Mia E.-L. Chalmers, Katy Andreasen, Niels Bogdanovic, Nenad Wilcock, Gordon K. Cairns, Nigel J. Feuk, Lars Brookes, Anthony J. Love, Seth Blennow, Kaj Kehoe, Patrick G. Prince, Jonathan A. |
| description | Insulin degrading enzyme, encoded by
IDE, plays a primary role in the degradation of amyloid β-protein (Aβ), the deposition of which in senile plaques is one of the defining hallmarks of Alzheimer's disease (AD). We recently identified haplotypes in a broad linkage disequilibrium (LD) block encompassing
IDE that associate with several AD-related quantitative traits. Here, by examining 32 polymorphic markers extending across
IDE and testing quantitative measures of plaque density and cognitive function in three independent Swedish AD samples, we have refined the probable position of pathogenic sequences to a 3′ region of
IDE, with local maximum effects in the proximity of marker rs1887922. To replicate these findings, a subset of variants were examined against measures of brain Aβ load in an independent English AD sample, whereby maximum effects were again observed for rs1887922. For both Swedish and English autopsy materials, variation at rs1887922 explained approximately 10% of the total variance in the respective histopathology traits. However, across all clinical materials studied to date, this variant site does not appear to associate directly with disease, suggesting that IDE may affect AD severity rather than risk. Results indicate that alleles of
IDE contribute to variability in Aβ deposition in the AD brain and suggest that this relationship may have relevance for the degree of cognitive dysfunction in AD patients. |
| doi_str_mv | 10.1016/j.neurobiolaging.2004.07.011 |
| format | Article |
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IDE, plays a primary role in the degradation of amyloid β-protein (Aβ), the deposition of which in senile plaques is one of the defining hallmarks of Alzheimer's disease (AD). We recently identified haplotypes in a broad linkage disequilibrium (LD) block encompassing
IDE that associate with several AD-related quantitative traits. Here, by examining 32 polymorphic markers extending across
IDE and testing quantitative measures of plaque density and cognitive function in three independent Swedish AD samples, we have refined the probable position of pathogenic sequences to a 3′ region of
IDE, with local maximum effects in the proximity of marker rs1887922. To replicate these findings, a subset of variants were examined against measures of brain Aβ load in an independent English AD sample, whereby maximum effects were again observed for rs1887922. For both Swedish and English autopsy materials, variation at rs1887922 explained approximately 10% of the total variance in the respective histopathology traits. However, across all clinical materials studied to date, this variant site does not appear to associate directly with disease, suggesting that IDE may affect AD severity rather than risk. Results indicate that alleles of
IDE contribute to variability in Aβ deposition in the AD brain and suggest that this relationship may have relevance for the degree of cognitive dysfunction in AD patients.</description><identifier>ISSN: 0197-4580</identifier><identifier>EISSN: 1558-1497</identifier><identifier>DOI: 10.1016/j.neurobiolaging.2004.07.011</identifier><identifier>PMID: 15718037</identifier><identifier>CODEN: NEAGDO</identifier><language>eng</language><publisher>London: Elsevier Inc</publisher><subject>a-beta ; Alzheimer Disease - epidemiology ; Alzheimer Disease - genetics ; Alzheimer Disease - metabolism ; Alzheimer's disease ; Amino Acid Sequence ; Amyloid beta-Peptides - genetics ; Amyloid beta-Peptides - metabolism ; Biological and medical sciences ; block spanning ide ; Brain - metabolism ; Chromosome Mapping - methods ; converting enzyme ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; DNA Mutational Analysis - methods ; England - epidemiology ; Genetic Markers - genetics ; Genetic Predisposition to Disease - epidemiology ; Genetic Variation ; Geriatrics ; Geriatrik ; Humans ; IDE ; in-vivo ; insulin-degrading enzyme ; Insulysin - genetics ; Insulysin - metabolism ; Linkage disequilibrium ; Linkage Disequilibrium - genetics ; Medical sciences ; missense mutations ; Molecular Sequence Data ; Mutation ; Neurology ; Neurosciences ; Neurovetenskaper ; onset ; plasma a-beta-42 ; protein ; Quantitative Trait Loci - genetics ; Statistics as Topic ; Sweden - epidemiology ; β-Amyloid</subject><ispartof>Neurobiology of aging, 2005-06, Vol.26 (6), p.795-802</ispartof><rights>2004 Elsevier Inc.</rights><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c489t-6683d5601f0ade1e7f85fe1ece831b3fb355d82fecbc5f13067d1311e033522a3</citedby><cites>FETCH-LOGICAL-c489t-6683d5601f0ade1e7f85fe1ece831b3fb355d82fecbc5f13067d1311e033522a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0197458004002854$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16558578$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15718037$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://gup.ub.gu.se/publication/80129$$DView record from Swedish Publication Index$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:1954875$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Blomqvist, Mia E.-L.</creatorcontrib><creatorcontrib>Chalmers, Katy</creatorcontrib><creatorcontrib>Andreasen, Niels</creatorcontrib><creatorcontrib>Bogdanovic, Nenad</creatorcontrib><creatorcontrib>Wilcock, Gordon K.</creatorcontrib><creatorcontrib>Cairns, Nigel J.</creatorcontrib><creatorcontrib>Feuk, Lars</creatorcontrib><creatorcontrib>Brookes, Anthony J.</creatorcontrib><creatorcontrib>Love, Seth</creatorcontrib><creatorcontrib>Blennow, Kaj</creatorcontrib><creatorcontrib>Kehoe, Patrick G.</creatorcontrib><creatorcontrib>Prince, Jonathan A.</creatorcontrib><title>Sequence variants of IDE are associated with the extent of β-amyloid deposition in the Alzheimer's disease brain</title><title>Neurobiology of aging</title><addtitle>Neurobiol Aging</addtitle><description>Insulin degrading enzyme, encoded by
IDE, plays a primary role in the degradation of amyloid β-protein (Aβ), the deposition of which in senile plaques is one of the defining hallmarks of Alzheimer's disease (AD). We recently identified haplotypes in a broad linkage disequilibrium (LD) block encompassing
IDE that associate with several AD-related quantitative traits. Here, by examining 32 polymorphic markers extending across
IDE and testing quantitative measures of plaque density and cognitive function in three independent Swedish AD samples, we have refined the probable position of pathogenic sequences to a 3′ region of
IDE, with local maximum effects in the proximity of marker rs1887922. To replicate these findings, a subset of variants were examined against measures of brain Aβ load in an independent English AD sample, whereby maximum effects were again observed for rs1887922. For both Swedish and English autopsy materials, variation at rs1887922 explained approximately 10% of the total variance in the respective histopathology traits. However, across all clinical materials studied to date, this variant site does not appear to associate directly with disease, suggesting that IDE may affect AD severity rather than risk. Results indicate that alleles of
IDE contribute to variability in Aβ deposition in the AD brain and suggest that this relationship may have relevance for the degree of cognitive dysfunction in AD patients.</description><subject>a-beta</subject><subject>Alzheimer Disease - epidemiology</subject><subject>Alzheimer Disease - genetics</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer's disease</subject><subject>Amino Acid Sequence</subject><subject>Amyloid beta-Peptides - genetics</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>Biological and medical sciences</subject><subject>block spanning ide</subject><subject>Brain - metabolism</subject><subject>Chromosome Mapping - methods</subject><subject>converting enzyme</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>DNA Mutational Analysis - methods</subject><subject>England - epidemiology</subject><subject>Genetic Markers - genetics</subject><subject>Genetic Predisposition to Disease - epidemiology</subject><subject>Genetic Variation</subject><subject>Geriatrics</subject><subject>Geriatrik</subject><subject>Humans</subject><subject>IDE</subject><subject>in-vivo</subject><subject>insulin-degrading enzyme</subject><subject>Insulysin - genetics</subject><subject>Insulysin - metabolism</subject><subject>Linkage disequilibrium</subject><subject>Linkage Disequilibrium - genetics</subject><subject>Medical sciences</subject><subject>missense mutations</subject><subject>Molecular Sequence Data</subject><subject>Mutation</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Neurovetenskaper</subject><subject>onset</subject><subject>plasma a-beta-42</subject><subject>protein</subject><subject>Quantitative Trait Loci - genetics</subject><subject>Statistics as Topic</subject><subject>Sweden - epidemiology</subject><subject>β-Amyloid</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>eNqN0s1u1DAQB3ALgehSeAXkAx8XsnjWcexIvVSlhUqVOABny7Enu16y8dZOWspj8SA8Ew4bUXFA4mTL-s3Ymr8JeQFsCQyqt9tlj2MMjQ-dWft-vVwxVi6ZXDKAB2QBQqgCylo-JAsGtSxKodgReZLSljEmS1k9JkcgJCjG5YJcf8LrEXuL9MZEb_oh0dDSy3fn1ESkJqVgvRnQ0Vs_bOiwQYrfBuyHSf38UZjdXRe8ow73IfnBh576_jc77b5v0O8wvk7U-YQmIW2i8f1T8qg1XcJn83pMvlycfz77UFx9fH95dnpV2FLVQ1FVijtRMWiZcQgoWyXavFpUHBreNlwIp1Yt2saKFjirpAMOgIxzsVoZfkyKQ990i_ux0fvodybe6WC8no--5h1qoaCuZfZv_unX417no_U4ecVgVWf-6sD3MeQJpkHvfLLYdabHMCZdybKEmlcZnhygjSGliO2fzsD0lKje6r8T1VOimkmdE83lz-d7xmaH7r54jjCDlzMwyZqujaa3Pt27Kn8IIVV2FweHeeg3HqNO1k_JOx_RDtoF_38v-gW7Y8r4</recordid><startdate>20050601</startdate><enddate>20050601</enddate><creator>Blomqvist, Mia E.-L.</creator><creator>Chalmers, Katy</creator><creator>Andreasen, Niels</creator><creator>Bogdanovic, Nenad</creator><creator>Wilcock, Gordon K.</creator><creator>Cairns, Nigel J.</creator><creator>Feuk, Lars</creator><creator>Brookes, Anthony J.</creator><creator>Love, Seth</creator><creator>Blennow, Kaj</creator><creator>Kehoe, Patrick G.</creator><creator>Prince, Jonathan A.</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><scope>ADTPV</scope><scope>AOWAS</scope><scope>F1U</scope></search><sort><creationdate>20050601</creationdate><title>Sequence variants of IDE are associated with the extent of β-amyloid deposition in the Alzheimer's disease brain</title><author>Blomqvist, Mia E.-L. ; Chalmers, Katy ; Andreasen, Niels ; Bogdanovic, Nenad ; Wilcock, Gordon K. ; Cairns, Nigel J. ; Feuk, Lars ; Brookes, Anthony J. ; Love, Seth ; Blennow, Kaj ; Kehoe, Patrick G. ; Prince, Jonathan A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c489t-6683d5601f0ade1e7f85fe1ece831b3fb355d82fecbc5f13067d1311e033522a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>a-beta</topic><topic>Alzheimer Disease - epidemiology</topic><topic>Alzheimer Disease - genetics</topic><topic>Alzheimer Disease - metabolism</topic><topic>Alzheimer's disease</topic><topic>Amino Acid Sequence</topic><topic>Amyloid beta-Peptides - genetics</topic><topic>Amyloid beta-Peptides - metabolism</topic><topic>Biological and medical sciences</topic><topic>block spanning ide</topic><topic>Brain - metabolism</topic><topic>Chromosome Mapping - methods</topic><topic>converting enzyme</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>DNA Mutational Analysis - methods</topic><topic>England - epidemiology</topic><topic>Genetic Markers - genetics</topic><topic>Genetic Predisposition to Disease - epidemiology</topic><topic>Genetic Variation</topic><topic>Geriatrics</topic><topic>Geriatrik</topic><topic>Humans</topic><topic>IDE</topic><topic>in-vivo</topic><topic>insulin-degrading enzyme</topic><topic>Insulysin - genetics</topic><topic>Insulysin - metabolism</topic><topic>Linkage disequilibrium</topic><topic>Linkage Disequilibrium - genetics</topic><topic>Medical sciences</topic><topic>missense mutations</topic><topic>Molecular Sequence Data</topic><topic>Mutation</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Neurovetenskaper</topic><topic>onset</topic><topic>plasma a-beta-42</topic><topic>protein</topic><topic>Quantitative Trait Loci - genetics</topic><topic>Statistics as Topic</topic><topic>Sweden - epidemiology</topic><topic>β-Amyloid</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Blomqvist, Mia E.-L.</creatorcontrib><creatorcontrib>Chalmers, Katy</creatorcontrib><creatorcontrib>Andreasen, Niels</creatorcontrib><creatorcontrib>Bogdanovic, Nenad</creatorcontrib><creatorcontrib>Wilcock, Gordon K.</creatorcontrib><creatorcontrib>Cairns, Nigel J.</creatorcontrib><creatorcontrib>Feuk, Lars</creatorcontrib><creatorcontrib>Brookes, Anthony J.</creatorcontrib><creatorcontrib>Love, Seth</creatorcontrib><creatorcontrib>Blennow, Kaj</creatorcontrib><creatorcontrib>Kehoe, Patrick G.</creatorcontrib><creatorcontrib>Prince, Jonathan A.</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><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Göteborgs universitet</collection><jtitle>Neurobiology of aging</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Blomqvist, Mia E.-L.</au><au>Chalmers, Katy</au><au>Andreasen, Niels</au><au>Bogdanovic, Nenad</au><au>Wilcock, Gordon K.</au><au>Cairns, Nigel J.</au><au>Feuk, Lars</au><au>Brookes, Anthony J.</au><au>Love, Seth</au><au>Blennow, Kaj</au><au>Kehoe, Patrick G.</au><au>Prince, Jonathan A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sequence variants of IDE are associated with the extent of β-amyloid deposition in the Alzheimer's disease brain</atitle><jtitle>Neurobiology of aging</jtitle><addtitle>Neurobiol Aging</addtitle><date>2005-06-01</date><risdate>2005</risdate><volume>26</volume><issue>6</issue><spage>795</spage><epage>802</epage><pages>795-802</pages><issn>0197-4580</issn><eissn>1558-1497</eissn><coden>NEAGDO</coden><abstract>Insulin degrading enzyme, encoded by
IDE, plays a primary role in the degradation of amyloid β-protein (Aβ), the deposition of which in senile plaques is one of the defining hallmarks of Alzheimer's disease (AD). We recently identified haplotypes in a broad linkage disequilibrium (LD) block encompassing
IDE that associate with several AD-related quantitative traits. Here, by examining 32 polymorphic markers extending across
IDE and testing quantitative measures of plaque density and cognitive function in three independent Swedish AD samples, we have refined the probable position of pathogenic sequences to a 3′ region of
IDE, with local maximum effects in the proximity of marker rs1887922. To replicate these findings, a subset of variants were examined against measures of brain Aβ load in an independent English AD sample, whereby maximum effects were again observed for rs1887922. For both Swedish and English autopsy materials, variation at rs1887922 explained approximately 10% of the total variance in the respective histopathology traits. However, across all clinical materials studied to date, this variant site does not appear to associate directly with disease, suggesting that IDE may affect AD severity rather than risk. Results indicate that alleles of
IDE contribute to variability in Aβ deposition in the AD brain and suggest that this relationship may have relevance for the degree of cognitive dysfunction in AD patients.</abstract><cop>London</cop><pub>Elsevier Inc</pub><pmid>15718037</pmid><doi>10.1016/j.neurobiolaging.2004.07.011</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Neurobiology of aging, 2005-06, Vol.26 (6), p.795-802 |
| issn | 0197-4580 1558-1497 |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | a-beta Alzheimer Disease - epidemiology Alzheimer Disease - genetics Alzheimer Disease - metabolism Alzheimer's disease Amino Acid Sequence Amyloid beta-Peptides - genetics Amyloid beta-Peptides - metabolism Biological and medical sciences block spanning ide Brain - metabolism Chromosome Mapping - methods converting enzyme Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases DNA Mutational Analysis - methods England - epidemiology Genetic Markers - genetics Genetic Predisposition to Disease - epidemiology Genetic Variation Geriatrics Geriatrik Humans IDE in-vivo insulin-degrading enzyme Insulysin - genetics Insulysin - metabolism Linkage disequilibrium Linkage Disequilibrium - genetics Medical sciences missense mutations Molecular Sequence Data Mutation Neurology Neurosciences Neurovetenskaper onset plasma a-beta-42 protein Quantitative Trait Loci - genetics Statistics as Topic Sweden - epidemiology β-Amyloid |
| title | Sequence variants of IDE are associated with the extent of β-amyloid deposition in the Alzheimer's disease brain |
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