Cardiovascular health, genetic risk, and risk of dementia in the Framingham Heart Study
OBJECTIVETo determine the joint role of ideal cardiovascular health (CVH) and genetic risk on risk of dementia. METHODSWe categorized CVH on the basis of the American Heart Association Ideal CVH Index and genetic risk through a genetic risk score (GRS) of common genetic variants and the APOE ε4 geno...
Gespeichert in:
Veröffentlicht in: | Neurology 2020-09, Vol.95 (10), p.e1341-e1350 |
---|---|
Hauptverfasser: | , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | e1350 |
---|---|
container_issue | 10 |
container_start_page | e1341 |
container_title | Neurology |
container_volume | 95 |
creator | Peloso, Gina M. Beiser, Alexa S. Satizabal, Claudia L. Xanthakis, Vanessa Vasan, Ramachandran S. Pase, Matthew P. Destefano, Anita L. Seshadri, Sudha |
description | OBJECTIVETo determine the joint role of ideal cardiovascular health (CVH) and genetic risk on risk of dementia.
METHODSWe categorized CVH on the basis of the American Heart Association Ideal CVH Index and genetic risk through a genetic risk score (GRS) of common genetic variants and the APOE ε4 genotype in 1,211 Framingham Heart Study (FHS) offspring cohort participants. We used multivariable Cox proportional hazards regression models to examine the association between CVH, genetic risk, and incident all-cause dementia with up to 10 years of follow-up (mean 8.4 years, 96 incident dementia cases), adjusting for age, sex, and education.
RESULTSWe observed that a high GRS (>80th percentile) was associated with a 2.6-fold risk of dementia (95% confidence interval [CI] of hazard ratio [HR] 1.23–5.29; p = 0.012) compared with having a low GRS ( |
doi_str_mv | 10.1212/WNL.0000000000010306 |
format | Article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmed_primary_32690788</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2425894940</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5026-dd671578bbf2d42916f9eba08325b36ba3baf765823ad428e068150b0f3bb22b3</originalsourceid><addsrcrecordid>eNqFkUtv1DAUhS0EokPhHyDkJYumXF8njrNBQqOWVhrBAlDZWdeJMzHNo9hJq_57PExbHgvwxpbvd8490mHspYBjgQLfXHzYHMOvI0CCesRWokCVKYlfH7MVAOpM6lIfsGcxfktQgWX1lB1IVBWUWq_YxZpC46drivXSU-Cdo37ujvjWjW72NQ8-Xh5xGpufLz61vHGDG2dP3I987hw_DTT4cdvRwM8chZl_mpfm9jl70lIf3Yu7-5B9OT35vD7LNh_fn6_fbbK6gBS0aVQpilJb22KTYyVUWzlLoCUWVipL0lJbqkKjpDTXDpQWBVhopbWIVh6yt3vfq8UOrqlTtEC9uQp-oHBrJvLmz8noO7Odrk1ZSI1CJoPXdwZh-r64OJvBx9r1PY1uWqLBHAtd5VUOCc33aB2mGINrH9YIMLtOTOrE_N1Jkr36PeKD6L6EBOg9cDP1swvxsl9uXDD7Kv7nnf9DuuOUEHmGgAAVaMh2X5X8ARPZqLI</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2425894940</pqid></control><display><type>article</type><title>Cardiovascular health, genetic risk, and risk of dementia in the Framingham Heart Study</title><source>MEDLINE</source><source>Journals@Ovid Ovid Autoload</source><source>Alma/SFX Local Collection</source><creator>Peloso, Gina M. ; Beiser, Alexa S. ; Satizabal, Claudia L. ; Xanthakis, Vanessa ; Vasan, Ramachandran S. ; Pase, Matthew P. ; Destefano, Anita L. ; Seshadri, Sudha</creator><creatorcontrib>Peloso, Gina M. ; Beiser, Alexa S. ; Satizabal, Claudia L. ; Xanthakis, Vanessa ; Vasan, Ramachandran S. ; Pase, Matthew P. ; Destefano, Anita L. ; Seshadri, Sudha</creatorcontrib><description>OBJECTIVETo determine the joint role of ideal cardiovascular health (CVH) and genetic risk on risk of dementia.
METHODSWe categorized CVH on the basis of the American Heart Association Ideal CVH Index and genetic risk through a genetic risk score (GRS) of common genetic variants and the APOE ε4 genotype in 1,211 Framingham Heart Study (FHS) offspring cohort participants. We used multivariable Cox proportional hazards regression models to examine the association between CVH, genetic risk, and incident all-cause dementia with up to 10 years of follow-up (mean 8.4 years, 96 incident dementia cases), adjusting for age, sex, and education.
RESULTSWe observed that a high GRS (>80th percentile) was associated with a 2.6-fold risk of dementia (95% confidence interval [CI] of hazard ratio [HR] 1.23–5.29; p = 0.012) compared with having a low GRS (<20th percentile); carrying at least 1 APOE ε4 allele was associated with a 2.3-fold risk of dementia compared with not carrying an APOE ε4 allele (95% CI of HR 1.49–3.53; p = 0.0002), and having a favorable CVH showed a 0.45-fold lower risk of dementia (95% CI of HR 0.20–1.01; p = 0.0527) compared to having an unfavorable CVH when all 3 components were included in the model. We did not observe an interaction between CVH and GRS (p = 0.99) or APOE ε4 (p = 0.16).
CONCLUSIONSWe observed that both genetic risk and CVH contribute additively to dementia risk.</description><identifier>ISSN: 0028-3878</identifier><identifier>EISSN: 1526-632X</identifier><identifier>DOI: 10.1212/WNL.0000000000010306</identifier><identifier>PMID: 32690788</identifier><language>eng</language><publisher>United States: American Academy of Neurology</publisher><subject>Aged ; Cardiovascular Diseases - complications ; Cardiovascular Diseases - epidemiology ; Comorbidity ; Dementia - epidemiology ; Dementia - etiology ; Female ; Genetic Predisposition to Disease ; Humans ; Incidence ; Longitudinal Studies ; Male ; Middle Aged ; Risk Factors</subject><ispartof>Neurology, 2020-09, Vol.95 (10), p.e1341-e1350</ispartof><rights>American Academy of Neurology</rights><rights>2020 American Academy of Neurology</rights><rights>2020 American Academy of Neurology.</rights><rights>2020 American Academy of Neurology 2020 American Academy of Neurology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5026-dd671578bbf2d42916f9eba08325b36ba3baf765823ad428e068150b0f3bb22b3</citedby><cites>FETCH-LOGICAL-c5026-dd671578bbf2d42916f9eba08325b36ba3baf765823ad428e068150b0f3bb22b3</cites><orcidid>0000-0002-1115-4430</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,777,781,882,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32690788$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Peloso, Gina M.</creatorcontrib><creatorcontrib>Beiser, Alexa S.</creatorcontrib><creatorcontrib>Satizabal, Claudia L.</creatorcontrib><creatorcontrib>Xanthakis, Vanessa</creatorcontrib><creatorcontrib>Vasan, Ramachandran S.</creatorcontrib><creatorcontrib>Pase, Matthew P.</creatorcontrib><creatorcontrib>Destefano, Anita L.</creatorcontrib><creatorcontrib>Seshadri, Sudha</creatorcontrib><title>Cardiovascular health, genetic risk, and risk of dementia in the Framingham Heart Study</title><title>Neurology</title><addtitle>Neurology</addtitle><description>OBJECTIVETo determine the joint role of ideal cardiovascular health (CVH) and genetic risk on risk of dementia.
METHODSWe categorized CVH on the basis of the American Heart Association Ideal CVH Index and genetic risk through a genetic risk score (GRS) of common genetic variants and the APOE ε4 genotype in 1,211 Framingham Heart Study (FHS) offspring cohort participants. We used multivariable Cox proportional hazards regression models to examine the association between CVH, genetic risk, and incident all-cause dementia with up to 10 years of follow-up (mean 8.4 years, 96 incident dementia cases), adjusting for age, sex, and education.
RESULTSWe observed that a high GRS (>80th percentile) was associated with a 2.6-fold risk of dementia (95% confidence interval [CI] of hazard ratio [HR] 1.23–5.29; p = 0.012) compared with having a low GRS (<20th percentile); carrying at least 1 APOE ε4 allele was associated with a 2.3-fold risk of dementia compared with not carrying an APOE ε4 allele (95% CI of HR 1.49–3.53; p = 0.0002), and having a favorable CVH showed a 0.45-fold lower risk of dementia (95% CI of HR 0.20–1.01; p = 0.0527) compared to having an unfavorable CVH when all 3 components were included in the model. We did not observe an interaction between CVH and GRS (p = 0.99) or APOE ε4 (p = 0.16).
CONCLUSIONSWe observed that both genetic risk and CVH contribute additively to dementia risk.</description><subject>Aged</subject><subject>Cardiovascular Diseases - complications</subject><subject>Cardiovascular Diseases - epidemiology</subject><subject>Comorbidity</subject><subject>Dementia - epidemiology</subject><subject>Dementia - etiology</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>Humans</subject><subject>Incidence</subject><subject>Longitudinal Studies</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Risk Factors</subject><issn>0028-3878</issn><issn>1526-632X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUtv1DAUhS0EokPhHyDkJYumXF8njrNBQqOWVhrBAlDZWdeJMzHNo9hJq_57PExbHgvwxpbvd8490mHspYBjgQLfXHzYHMOvI0CCesRWokCVKYlfH7MVAOpM6lIfsGcxfktQgWX1lB1IVBWUWq_YxZpC46drivXSU-Cdo37ujvjWjW72NQ8-Xh5xGpufLz61vHGDG2dP3I987hw_DTT4cdvRwM8chZl_mpfm9jl70lIf3Yu7-5B9OT35vD7LNh_fn6_fbbK6gBS0aVQpilJb22KTYyVUWzlLoCUWVipL0lJbqkKjpDTXDpQWBVhopbWIVh6yt3vfq8UOrqlTtEC9uQp-oHBrJvLmz8noO7Odrk1ZSI1CJoPXdwZh-r64OJvBx9r1PY1uWqLBHAtd5VUOCc33aB2mGINrH9YIMLtOTOrE_N1Jkr36PeKD6L6EBOg9cDP1swvxsl9uXDD7Kv7nnf9DuuOUEHmGgAAVaMh2X5X8ARPZqLI</recordid><startdate>20200908</startdate><enddate>20200908</enddate><creator>Peloso, Gina M.</creator><creator>Beiser, Alexa S.</creator><creator>Satizabal, Claudia L.</creator><creator>Xanthakis, Vanessa</creator><creator>Vasan, Ramachandran S.</creator><creator>Pase, Matthew P.</creator><creator>Destefano, Anita L.</creator><creator>Seshadri, Sudha</creator><general>American Academy of Neurology</general><general>Lippincott Williams & Wilkins</general><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>5PM</scope><orcidid>https://orcid.org/0000-0002-1115-4430</orcidid></search><sort><creationdate>20200908</creationdate><title>Cardiovascular health, genetic risk, and risk of dementia in the Framingham Heart Study</title><author>Peloso, Gina M. ; Beiser, Alexa S. ; Satizabal, Claudia L. ; Xanthakis, Vanessa ; Vasan, Ramachandran S. ; Pase, Matthew P. ; Destefano, Anita L. ; Seshadri, Sudha</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5026-dd671578bbf2d42916f9eba08325b36ba3baf765823ad428e068150b0f3bb22b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Aged</topic><topic>Cardiovascular Diseases - complications</topic><topic>Cardiovascular Diseases - epidemiology</topic><topic>Comorbidity</topic><topic>Dementia - epidemiology</topic><topic>Dementia - etiology</topic><topic>Female</topic><topic>Genetic Predisposition to Disease</topic><topic>Humans</topic><topic>Incidence</topic><topic>Longitudinal Studies</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Risk Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Peloso, Gina M.</creatorcontrib><creatorcontrib>Beiser, Alexa S.</creatorcontrib><creatorcontrib>Satizabal, Claudia L.</creatorcontrib><creatorcontrib>Xanthakis, Vanessa</creatorcontrib><creatorcontrib>Vasan, Ramachandran S.</creatorcontrib><creatorcontrib>Pase, Matthew P.</creatorcontrib><creatorcontrib>Destefano, Anita L.</creatorcontrib><creatorcontrib>Seshadri, Sudha</creatorcontrib><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>PubMed Central (Full Participant titles)</collection><jtitle>Neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Peloso, Gina M.</au><au>Beiser, Alexa S.</au><au>Satizabal, Claudia L.</au><au>Xanthakis, Vanessa</au><au>Vasan, Ramachandran S.</au><au>Pase, Matthew P.</au><au>Destefano, Anita L.</au><au>Seshadri, Sudha</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cardiovascular health, genetic risk, and risk of dementia in the Framingham Heart Study</atitle><jtitle>Neurology</jtitle><addtitle>Neurology</addtitle><date>2020-09-08</date><risdate>2020</risdate><volume>95</volume><issue>10</issue><spage>e1341</spage><epage>e1350</epage><pages>e1341-e1350</pages><issn>0028-3878</issn><eissn>1526-632X</eissn><abstract>OBJECTIVETo determine the joint role of ideal cardiovascular health (CVH) and genetic risk on risk of dementia.
METHODSWe categorized CVH on the basis of the American Heart Association Ideal CVH Index and genetic risk through a genetic risk score (GRS) of common genetic variants and the APOE ε4 genotype in 1,211 Framingham Heart Study (FHS) offspring cohort participants. We used multivariable Cox proportional hazards regression models to examine the association between CVH, genetic risk, and incident all-cause dementia with up to 10 years of follow-up (mean 8.4 years, 96 incident dementia cases), adjusting for age, sex, and education.
RESULTSWe observed that a high GRS (>80th percentile) was associated with a 2.6-fold risk of dementia (95% confidence interval [CI] of hazard ratio [HR] 1.23–5.29; p = 0.012) compared with having a low GRS (<20th percentile); carrying at least 1 APOE ε4 allele was associated with a 2.3-fold risk of dementia compared with not carrying an APOE ε4 allele (95% CI of HR 1.49–3.53; p = 0.0002), and having a favorable CVH showed a 0.45-fold lower risk of dementia (95% CI of HR 0.20–1.01; p = 0.0527) compared to having an unfavorable CVH when all 3 components were included in the model. We did not observe an interaction between CVH and GRS (p = 0.99) or APOE ε4 (p = 0.16).
CONCLUSIONSWe observed that both genetic risk and CVH contribute additively to dementia risk.</abstract><cop>United States</cop><pub>American Academy of Neurology</pub><pmid>32690788</pmid><doi>10.1212/WNL.0000000000010306</doi><orcidid>https://orcid.org/0000-0002-1115-4430</orcidid><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0028-3878 |
ispartof | Neurology, 2020-09, Vol.95 (10), p.e1341-e1350 |
issn | 0028-3878 1526-632X |
language | eng |
recordid | cdi_pubmed_primary_32690788 |
source | MEDLINE; Journals@Ovid Ovid Autoload; Alma/SFX Local Collection |
subjects | Aged Cardiovascular Diseases - complications Cardiovascular Diseases - epidemiology Comorbidity Dementia - epidemiology Dementia - etiology Female Genetic Predisposition to Disease Humans Incidence Longitudinal Studies Male Middle Aged Risk Factors |
title | Cardiovascular health, genetic risk, and risk of dementia in the Framingham Heart Study |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-18T18%3A40%3A10IST&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=Cardiovascular%20health,%20genetic%20risk,%20and%20risk%20of%20dementia%20in%20the%20Framingham%20Heart%20Study&rft.jtitle=Neurology&rft.au=Peloso,%20Gina%20M.&rft.date=2020-09-08&rft.volume=95&rft.issue=10&rft.spage=e1341&rft.epage=e1350&rft.pages=e1341-e1350&rft.issn=0028-3878&rft.eissn=1526-632X&rft_id=info:doi/10.1212/WNL.0000000000010306&rft_dat=%3Cproquest_pubme%3E2425894940%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=2425894940&rft_id=info:pmid/32690788&rfr_iscdi=true |