CR1 is associated with amyloid plaque burden and age-related cognitive decline
Objective Recently, genome‐wide association studies have identified 3 new susceptibility loci for Alzheimer's disease (AD), CLU, CR1, and PICALM. We leveraged available neuropsychological and autopsy data from 2 cohort studies to investigate whether these loci are associated with cognitive decl...
Gespeichert in:
| Veröffentlicht in: | Annals of neurology 2011-03, Vol.69 (3), p.560-569 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 569 |
|---|---|
| container_issue | 3 |
| container_start_page | 560 |
| container_title | Annals of neurology |
| container_volume | 69 |
| creator | Chibnik, Lori B. Shulman, Joshua M. Leurgans, Sue E. Schneider, Julie A. Wilson, Robert S. Tran, Dong Aubin, Cristin Buchman, Aron S. Heward, Christopher B. Myers, Amanda J. Hardy, John A. Huentelman, Matthew J. Corneveaux, Jason J. Reiman, Eric M. Evans, Denis A. Bennett, David A. De Jager, Philip L. |
| description | Objective
Recently, genome‐wide association studies have identified 3 new susceptibility loci for Alzheimer's disease (AD), CLU, CR1, and PICALM. We leveraged available neuropsychological and autopsy data from 2 cohort studies to investigate whether these loci are associated with cognitive decline and AD neuropathology.
Methods
The Religious Orders Study (ROS) and Rush Memory and Aging Project (MAP) are longitudinal studies that enroll nondemented subjects and include annual clinical evaluations and brain donation at death. We evaluated CR1 (rs6656401), CLU (rs11136000), and PICALM (rs7110631) in 1,666 subjects. We evaluated associations between genotypes and rate of change in cognitive function as well as AD‐related pathology. Lastly, we used pathway analysis to determine whether relationships between single nucleotide polymorphisms and cognitive decline are mediated through AD pathology.
Results
Among our study cohort, the mean years of follow‐up were 7.8 for ROS and 4.3 for MAP. Only the CR1 locus was associated with both global cognitive decline (p = 0.011) and global AD pathology (p = 0.025). More specifically, the locus affects the deposition of neuritic amyloid plaque (p = 0.009). In a mediation analysis, controlling for amyloid pathology strongly attenuated the effect of the CR1 locus on cognitive decline.
Interpretation
We found that common variation at the CR1 locus has a broad impact on cognition and that this effect is largely mediated by an individual's amyloid plaque burden. We therefore highlight 1 functional consequence of the CR1 susceptibility allele and generalize the role of this locus to cognitive aging in the general population. ANN NEUROL 2011 |
| doi_str_mv | 10.1002/ana.22277 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3066288</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>859314295</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5427-e03dd84ec7eb92af0587403cc686e59249006bab17f21ec06e34faca02f6d80c3</originalsourceid><addsrcrecordid>eNqFkk1v1DAQhi0EosvCgT-AIiGEOKQd24njXCotKyiIslR8iKM1cSZbF2-y2EnL_nvS7nb5kBCnOcwz77zj14w95nDIAcQRtngohCiKO2zCc8lTLbLyLpuAVFmac5kdsAcxXgBAqTjcZweCy5ILKSZsMf_IExcTjLGzDnuqkyvXnye42vjO1cna4_eBkmoINbUJtnWCS0oD-RvUdsvW9e6Skpqsdy09ZPca9JEe7eqUfXn96vP8TXr64eTtfHaa2jwTRUog61pnZAuqSoEN5LrIQFqrtKK8HN0DqAorXjSCkwVFMmvQIohG1RqsnLLjre56qFZUW2r7gN6sg1th2JgOnfmz07pzs-wujQSlhNajwPOdQOjGA2NvVi5a8h5b6oZotNYcxLWp_5J5KXkmynwkn_5FXnRDaMd3MFwWUgglSzFSL7aUDV2MgZq9aw7mOk4zxmlu4hzZJ7-fuSdv8xuBZzsAo0XfBGyti7-4DISG8QdM2dGWu3KeNv_eaGaL2e3qdDvhYk8_9hMYvhlVyCI3Xxcn5ix_efbuU_beaPkTycjEtQ</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1373226392</pqid></control><display><type>article</type><title>CR1 is associated with amyloid plaque burden and age-related cognitive decline</title><source>MEDLINE</source><source>Wiley Online Library All Journals</source><creator>Chibnik, Lori B. ; Shulman, Joshua M. ; Leurgans, Sue E. ; Schneider, Julie A. ; Wilson, Robert S. ; Tran, Dong ; Aubin, Cristin ; Buchman, Aron S. ; Heward, Christopher B. ; Myers, Amanda J. ; Hardy, John A. ; Huentelman, Matthew J. ; Corneveaux, Jason J. ; Reiman, Eric M. ; Evans, Denis A. ; Bennett, David A. ; De Jager, Philip L.</creator><creatorcontrib>Chibnik, Lori B. ; Shulman, Joshua M. ; Leurgans, Sue E. ; Schneider, Julie A. ; Wilson, Robert S. ; Tran, Dong ; Aubin, Cristin ; Buchman, Aron S. ; Heward, Christopher B. ; Myers, Amanda J. ; Hardy, John A. ; Huentelman, Matthew J. ; Corneveaux, Jason J. ; Reiman, Eric M. ; Evans, Denis A. ; Bennett, David A. ; De Jager, Philip L.</creatorcontrib><description>Objective
Recently, genome‐wide association studies have identified 3 new susceptibility loci for Alzheimer's disease (AD), CLU, CR1, and PICALM. We leveraged available neuropsychological and autopsy data from 2 cohort studies to investigate whether these loci are associated with cognitive decline and AD neuropathology.
Methods
The Religious Orders Study (ROS) and Rush Memory and Aging Project (MAP) are longitudinal studies that enroll nondemented subjects and include annual clinical evaluations and brain donation at death. We evaluated CR1 (rs6656401), CLU (rs11136000), and PICALM (rs7110631) in 1,666 subjects. We evaluated associations between genotypes and rate of change in cognitive function as well as AD‐related pathology. Lastly, we used pathway analysis to determine whether relationships between single nucleotide polymorphisms and cognitive decline are mediated through AD pathology.
Results
Among our study cohort, the mean years of follow‐up were 7.8 for ROS and 4.3 for MAP. Only the CR1 locus was associated with both global cognitive decline (p = 0.011) and global AD pathology (p = 0.025). More specifically, the locus affects the deposition of neuritic amyloid plaque (p = 0.009). In a mediation analysis, controlling for amyloid pathology strongly attenuated the effect of the CR1 locus on cognitive decline.
Interpretation
We found that common variation at the CR1 locus has a broad impact on cognition and that this effect is largely mediated by an individual's amyloid plaque burden. We therefore highlight 1 functional consequence of the CR1 susceptibility allele and generalize the role of this locus to cognitive aging in the general population. ANN NEUROL 2011</description><identifier>ISSN: 0364-5134</identifier><identifier>EISSN: 1531-8249</identifier><identifier>DOI: 10.1002/ana.22277</identifier><identifier>PMID: 21391232</identifier><identifier>CODEN: ANNED3</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Age Factors ; Aged ; Aged, 80 and over ; Alleles ; Alzheimer Disease - genetics ; Alzheimer Disease - metabolism ; Alzheimer Disease - pathology ; Alzheimer's disease ; Analysis of Variance ; Biological and medical sciences ; Brain - metabolism ; Brain - pathology ; Cognition & reasoning ; Cognition Disorders - genetics ; Cognition Disorders - metabolism ; Cognition Disorders - pathology ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Female ; Genetic Association Studies ; Genetic Predisposition to Disease ; Genetics ; Genotype ; Humans ; Longitudinal Studies ; Male ; Medical sciences ; Middle Aged ; Neurology ; Pathology ; Plaque, Amyloid - genetics ; Plaque, Amyloid - metabolism ; Plaque, Amyloid - pathology ; Polymorphism, Single Nucleotide ; Receptors, Complement 3b - genetics ; Receptors, Complement 3b - metabolism ; Religious orders</subject><ispartof>Annals of neurology, 2011-03, Vol.69 (3), p.560-569</ispartof><rights>Copyright © 2011 American Neurological Association</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2011 American Neurological Association.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5427-e03dd84ec7eb92af0587403cc686e59249006bab17f21ec06e34faca02f6d80c3</citedby><cites>FETCH-LOGICAL-c5427-e03dd84ec7eb92af0587403cc686e59249006bab17f21ec06e34faca02f6d80c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fana.22277$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fana.22277$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,780,784,885,1417,27923,27924,45573,45574</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24028051$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21391232$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chibnik, Lori B.</creatorcontrib><creatorcontrib>Shulman, Joshua M.</creatorcontrib><creatorcontrib>Leurgans, Sue E.</creatorcontrib><creatorcontrib>Schneider, Julie A.</creatorcontrib><creatorcontrib>Wilson, Robert S.</creatorcontrib><creatorcontrib>Tran, Dong</creatorcontrib><creatorcontrib>Aubin, Cristin</creatorcontrib><creatorcontrib>Buchman, Aron S.</creatorcontrib><creatorcontrib>Heward, Christopher B.</creatorcontrib><creatorcontrib>Myers, Amanda J.</creatorcontrib><creatorcontrib>Hardy, John A.</creatorcontrib><creatorcontrib>Huentelman, Matthew J.</creatorcontrib><creatorcontrib>Corneveaux, Jason J.</creatorcontrib><creatorcontrib>Reiman, Eric M.</creatorcontrib><creatorcontrib>Evans, Denis A.</creatorcontrib><creatorcontrib>Bennett, David A.</creatorcontrib><creatorcontrib>De Jager, Philip L.</creatorcontrib><title>CR1 is associated with amyloid plaque burden and age-related cognitive decline</title><title>Annals of neurology</title><addtitle>Ann Neurol</addtitle><description>Objective
Recently, genome‐wide association studies have identified 3 new susceptibility loci for Alzheimer's disease (AD), CLU, CR1, and PICALM. We leveraged available neuropsychological and autopsy data from 2 cohort studies to investigate whether these loci are associated with cognitive decline and AD neuropathology.
Methods
The Religious Orders Study (ROS) and Rush Memory and Aging Project (MAP) are longitudinal studies that enroll nondemented subjects and include annual clinical evaluations and brain donation at death. We evaluated CR1 (rs6656401), CLU (rs11136000), and PICALM (rs7110631) in 1,666 subjects. We evaluated associations between genotypes and rate of change in cognitive function as well as AD‐related pathology. Lastly, we used pathway analysis to determine whether relationships between single nucleotide polymorphisms and cognitive decline are mediated through AD pathology.
Results
Among our study cohort, the mean years of follow‐up were 7.8 for ROS and 4.3 for MAP. Only the CR1 locus was associated with both global cognitive decline (p = 0.011) and global AD pathology (p = 0.025). More specifically, the locus affects the deposition of neuritic amyloid plaque (p = 0.009). In a mediation analysis, controlling for amyloid pathology strongly attenuated the effect of the CR1 locus on cognitive decline.
Interpretation
We found that common variation at the CR1 locus has a broad impact on cognition and that this effect is largely mediated by an individual's amyloid plaque burden. We therefore highlight 1 functional consequence of the CR1 susceptibility allele and generalize the role of this locus to cognitive aging in the general population. ANN NEUROL 2011</description><subject>Age Factors</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Alleles</subject><subject>Alzheimer Disease - genetics</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer Disease - pathology</subject><subject>Alzheimer's disease</subject><subject>Analysis of Variance</subject><subject>Biological and medical sciences</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Cognition & reasoning</subject><subject>Cognition Disorders - genetics</subject><subject>Cognition Disorders - metabolism</subject><subject>Cognition Disorders - pathology</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Female</subject><subject>Genetic Association Studies</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetics</subject><subject>Genotype</subject><subject>Humans</subject><subject>Longitudinal Studies</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Neurology</subject><subject>Pathology</subject><subject>Plaque, Amyloid - genetics</subject><subject>Plaque, Amyloid - metabolism</subject><subject>Plaque, Amyloid - pathology</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Receptors, Complement 3b - genetics</subject><subject>Receptors, Complement 3b - metabolism</subject><subject>Religious orders</subject><issn>0364-5134</issn><issn>1531-8249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkk1v1DAQhi0EosvCgT-AIiGEOKQd24njXCotKyiIslR8iKM1cSZbF2-y2EnL_nvS7nb5kBCnOcwz77zj14w95nDIAcQRtngohCiKO2zCc8lTLbLyLpuAVFmac5kdsAcxXgBAqTjcZweCy5ILKSZsMf_IExcTjLGzDnuqkyvXnye42vjO1cna4_eBkmoINbUJtnWCS0oD-RvUdsvW9e6Skpqsdy09ZPca9JEe7eqUfXn96vP8TXr64eTtfHaa2jwTRUog61pnZAuqSoEN5LrIQFqrtKK8HN0DqAorXjSCkwVFMmvQIohG1RqsnLLjre56qFZUW2r7gN6sg1th2JgOnfmz07pzs-wujQSlhNajwPOdQOjGA2NvVi5a8h5b6oZotNYcxLWp_5J5KXkmynwkn_5FXnRDaMd3MFwWUgglSzFSL7aUDV2MgZq9aw7mOk4zxmlu4hzZJ7-fuSdv8xuBZzsAo0XfBGyti7-4DISG8QdM2dGWu3KeNv_eaGaL2e3qdDvhYk8_9hMYvhlVyCI3Xxcn5ix_efbuU_beaPkTycjEtQ</recordid><startdate>201103</startdate><enddate>201103</enddate><creator>Chibnik, Lori B.</creator><creator>Shulman, Joshua M.</creator><creator>Leurgans, Sue E.</creator><creator>Schneider, Julie A.</creator><creator>Wilson, Robert S.</creator><creator>Tran, Dong</creator><creator>Aubin, Cristin</creator><creator>Buchman, Aron S.</creator><creator>Heward, Christopher B.</creator><creator>Myers, Amanda J.</creator><creator>Hardy, John A.</creator><creator>Huentelman, Matthew J.</creator><creator>Corneveaux, Jason J.</creator><creator>Reiman, Eric M.</creator><creator>Evans, Denis A.</creator><creator>Bennett, David A.</creator><creator>De Jager, Philip L.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><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>7U7</scope><scope>C1K</scope><scope>K9.</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201103</creationdate><title>CR1 is associated with amyloid plaque burden and age-related cognitive decline</title><author>Chibnik, Lori B. ; Shulman, Joshua M. ; Leurgans, Sue E. ; Schneider, Julie A. ; Wilson, Robert S. ; Tran, Dong ; Aubin, Cristin ; Buchman, Aron S. ; Heward, Christopher B. ; Myers, Amanda J. ; Hardy, John A. ; Huentelman, Matthew J. ; Corneveaux, Jason J. ; Reiman, Eric M. ; Evans, Denis A. ; Bennett, David A. ; De Jager, Philip L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5427-e03dd84ec7eb92af0587403cc686e59249006bab17f21ec06e34faca02f6d80c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Age Factors</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Alleles</topic><topic>Alzheimer Disease - genetics</topic><topic>Alzheimer Disease - metabolism</topic><topic>Alzheimer Disease - pathology</topic><topic>Alzheimer's disease</topic><topic>Analysis of Variance</topic><topic>Biological and medical sciences</topic><topic>Brain - metabolism</topic><topic>Brain - pathology</topic><topic>Cognition & reasoning</topic><topic>Cognition Disorders - genetics</topic><topic>Cognition Disorders - metabolism</topic><topic>Cognition Disorders - pathology</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Female</topic><topic>Genetic Association Studies</topic><topic>Genetic Predisposition to Disease</topic><topic>Genetics</topic><topic>Genotype</topic><topic>Humans</topic><topic>Longitudinal Studies</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Neurology</topic><topic>Pathology</topic><topic>Plaque, Amyloid - genetics</topic><topic>Plaque, Amyloid - metabolism</topic><topic>Plaque, Amyloid - pathology</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Receptors, Complement 3b - genetics</topic><topic>Receptors, Complement 3b - metabolism</topic><topic>Religious orders</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chibnik, Lori B.</creatorcontrib><creatorcontrib>Shulman, Joshua M.</creatorcontrib><creatorcontrib>Leurgans, Sue E.</creatorcontrib><creatorcontrib>Schneider, Julie A.</creatorcontrib><creatorcontrib>Wilson, Robert S.</creatorcontrib><creatorcontrib>Tran, Dong</creatorcontrib><creatorcontrib>Aubin, Cristin</creatorcontrib><creatorcontrib>Buchman, Aron S.</creatorcontrib><creatorcontrib>Heward, Christopher B.</creatorcontrib><creatorcontrib>Myers, Amanda J.</creatorcontrib><creatorcontrib>Hardy, John A.</creatorcontrib><creatorcontrib>Huentelman, Matthew J.</creatorcontrib><creatorcontrib>Corneveaux, Jason J.</creatorcontrib><creatorcontrib>Reiman, Eric M.</creatorcontrib><creatorcontrib>Evans, Denis A.</creatorcontrib><creatorcontrib>Bennett, David A.</creatorcontrib><creatorcontrib>De Jager, Philip L.</creatorcontrib><collection>Istex</collection><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>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Annals of neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chibnik, Lori B.</au><au>Shulman, Joshua M.</au><au>Leurgans, Sue E.</au><au>Schneider, Julie A.</au><au>Wilson, Robert S.</au><au>Tran, Dong</au><au>Aubin, Cristin</au><au>Buchman, Aron S.</au><au>Heward, Christopher B.</au><au>Myers, Amanda J.</au><au>Hardy, John A.</au><au>Huentelman, Matthew J.</au><au>Corneveaux, Jason J.</au><au>Reiman, Eric M.</au><au>Evans, Denis A.</au><au>Bennett, David A.</au><au>De Jager, Philip L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CR1 is associated with amyloid plaque burden and age-related cognitive decline</atitle><jtitle>Annals of neurology</jtitle><addtitle>Ann Neurol</addtitle><date>2011-03</date><risdate>2011</risdate><volume>69</volume><issue>3</issue><spage>560</spage><epage>569</epage><pages>560-569</pages><issn>0364-5134</issn><eissn>1531-8249</eissn><coden>ANNED3</coden><abstract>Objective
Recently, genome‐wide association studies have identified 3 new susceptibility loci for Alzheimer's disease (AD), CLU, CR1, and PICALM. We leveraged available neuropsychological and autopsy data from 2 cohort studies to investigate whether these loci are associated with cognitive decline and AD neuropathology.
Methods
The Religious Orders Study (ROS) and Rush Memory and Aging Project (MAP) are longitudinal studies that enroll nondemented subjects and include annual clinical evaluations and brain donation at death. We evaluated CR1 (rs6656401), CLU (rs11136000), and PICALM (rs7110631) in 1,666 subjects. We evaluated associations between genotypes and rate of change in cognitive function as well as AD‐related pathology. Lastly, we used pathway analysis to determine whether relationships between single nucleotide polymorphisms and cognitive decline are mediated through AD pathology.
Results
Among our study cohort, the mean years of follow‐up were 7.8 for ROS and 4.3 for MAP. Only the CR1 locus was associated with both global cognitive decline (p = 0.011) and global AD pathology (p = 0.025). More specifically, the locus affects the deposition of neuritic amyloid plaque (p = 0.009). In a mediation analysis, controlling for amyloid pathology strongly attenuated the effect of the CR1 locus on cognitive decline.
Interpretation
We found that common variation at the CR1 locus has a broad impact on cognition and that this effect is largely mediated by an individual's amyloid plaque burden. We therefore highlight 1 functional consequence of the CR1 susceptibility allele and generalize the role of this locus to cognitive aging in the general population. ANN NEUROL 2011</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>21391232</pmid><doi>10.1002/ana.22277</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0364-5134 |
| ispartof | Annals of neurology, 2011-03, Vol.69 (3), p.560-569 |
| issn | 0364-5134 1531-8249 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3066288 |
| source | MEDLINE; Wiley Online Library All Journals |
| subjects | Age Factors Aged Aged, 80 and over Alleles Alzheimer Disease - genetics Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer's disease Analysis of Variance Biological and medical sciences Brain - metabolism Brain - pathology Cognition & reasoning Cognition Disorders - genetics Cognition Disorders - metabolism Cognition Disorders - pathology Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Female Genetic Association Studies Genetic Predisposition to Disease Genetics Genotype Humans Longitudinal Studies Male Medical sciences Middle Aged Neurology Pathology Plaque, Amyloid - genetics Plaque, Amyloid - metabolism Plaque, Amyloid - pathology Polymorphism, Single Nucleotide Receptors, Complement 3b - genetics Receptors, Complement 3b - metabolism Religious orders |
| title | CR1 is associated with amyloid plaque burden and age-related cognitive decline |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-08T08%3A20%3A16IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=CR1%20is%20associated%20with%20amyloid%20plaque%20burden%20and%20age-related%20cognitive%20decline&rft.jtitle=Annals%20of%20neurology&rft.au=Chibnik,%20Lori%20B.&rft.date=2011-03&rft.volume=69&rft.issue=3&rft.spage=560&rft.epage=569&rft.pages=560-569&rft.issn=0364-5134&rft.eissn=1531-8249&rft.coden=ANNED3&rft_id=info:doi/10.1002/ana.22277&rft_dat=%3Cproquest_pubme%3E859314295%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1373226392&rft_id=info:pmid/21391232&rfr_iscdi=true |