The impact of APOE genotype on survival: Results of 38,537 participants from six population-based cohorts (E2-CHARGE)
Apolipoprotein E is a glycoprotein best known as a mediator and regulator of lipid transport and uptake. The APOE-ε4 allele has long been associated with increased risks of Alzheimer's disease and mortality, but the effect of the less prevalent APOE-ε2 allele on diseases in the elderly and surv...
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| Vydáno v: | PloS one Ročník 14; číslo 7; s. e0219668 |
|---|---|
| Hlavní autoři: | , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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United States
Public Library of Science
29.07.2019
Public Library of Science (PLoS) |
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| ISSN: | 1932-6203, 1932-6203 |
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| Abstract | Apolipoprotein E is a glycoprotein best known as a mediator and regulator of lipid transport and uptake. The APOE-ε4 allele has long been associated with increased risks of Alzheimer's disease and mortality, but the effect of the less prevalent APOE-ε2 allele on diseases in the elderly and survival remains elusive.
We aggregated data of 38,537 individuals of European ancestry (mean age 65.5 years; 55.6% women) from six population-based cohort studies (Rotterdam Study, AGES-Reykjavik Study, Cardiovascular Health Study, Health-ABC Study, and the family-based Framingham Heart Study and Long Life Family Study) to determine the association of APOE, and in particular APOE-ε2, with survival in the population.
During a mean follow-up of 11.7 years, 17,021 individuals died. Compared with homozygous APOE-ε3 carriers, APOE-ε2 carriers were at lower risk of death (hazard ratio,95% confidence interval: 0.94,0.90-0.99; P = 1.1*10-2), whereas APOE-ε4 carriers were at increased risk of death (HR 1.17,1.12-1.21; P = 2.8*10-16). APOE was associated with mortality risk in a dose-dependent manner, with risk estimates lowest for homozygous APOE-ε2 (HR 0.89,0.74-1.08), and highest for homozygous APOE-ε4 (HR 1.52,1.37-1.70). After censoring for dementia, effect estimates remained similar for APOE-ε2 (HR 0.95,0.90-1.01), but attenuated for APOE-ε4 (HR 1.07,1.01-1.12). Results were broadly similar across cohorts, and did not differ by age or sex. APOE genotype was associated with baseline lipid fractions (e.g. mean difference(95%CI) in LDL(mg/dL) for ε2 versus ε33: -17.1(-18.1-16.0), and ε4 versus ε33: +5.7(4.8;6.5)), but the association between APOE and mortality was unaltered after adjustment for baseline LDL or cardiovascular disease. Given the European ancestry of the study population, results may not apply to other ethnicities.
Compared with APOE-ε3, APOE-ε2 is associated with prolonged survival, whereas mortality risk is increased for APOE-ε4 carriers. Further collaborative efforts are needed to unravel the role of APOE and in particular APOE-ε2 in health and disease. |
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| AbstractList | Background Apolipoprotein E is a glycoprotein best known as a mediator and regulator of lipid transport and uptake. The APOE-[epsilon]4 allele has long been associated with increased risks of Alzheimer's disease and mortality, but the effect of the less prevalent APOE-[epsilon]2 allele on diseases in the elderly and survival remains elusive. Methods We aggregated data of 38,537 individuals of European ancestry (mean age 65.5 years; 55.6% women) from six population-based cohort studies (Rotterdam Study, AGES-Reykjavik Study, Cardiovascular Health Study, Health-ABC Study, and the family-based Framingham Heart Study and Long Life Family Study) to determine the association of APOE, and in particular APOE-[epsilon]2, with survival in the population. Results During a mean follow-up of 11.7 years, 17,021 individuals died. Compared with homozygous APOE-[epsilon]3 carriers, APOE-[epsilon]2 carriers were at lower risk of death (hazard ratio,95% confidence interval: 0.94,0.90-0.99; P = 1.1*10.sup.-2 ), whereas APOE-[epsilon]4 carriers were at increased risk of death (HR 1.17,1.12-1.21; P = 2.8*10.sup.-16). APOE was associated with mortality risk in a dose-dependent manner, with risk estimates lowest for homozygous APOE-[epsilon]2 (HR 0.89,0.74-1.08), and highest for homozygous APOE-[epsilon]4 (HR 1.52,1.37-1.70). After censoring for dementia, effect estimates remained similar for APOE-[epsilon]2 (HR 0.95,0.90-1.01), but attenuated for APOE-[epsilon]4 (HR 1.07,1.01-1.12). Results were broadly similar across cohorts, and did not differ by age or sex. APOE genotype was associated with baseline lipid fractions (e.g. mean difference(95%CI) in LDL(mg/dL) for [epsilon]2 versus [epsilon]33: -17.1(-18.1-16.0), and [epsilon]4 versus [epsilon]33: +5.7(4.8;6.5)), but the association between APOE and mortality was unaltered after adjustment for baseline LDL or cardiovascular disease. Given the European ancestry of the study population, results may not apply to other ethnicities. Conclusion Compared with APOE-[epsilon]3, APOE-[epsilon]2 is associated with prolonged survival, whereas mortality risk is increased for APOE-[epsilon]4 carriers. Further collaborative efforts are needed to unravel the role of APOE and in particular APOE-[epsilon]2 in health and disease. Apolipoprotein E is a glycoprotein best known as a mediator and regulator of lipid transport and uptake. The APOE-[epsilon]4 allele has long been associated with increased risks of Alzheimer's disease and mortality, but the effect of the less prevalent APOE-[epsilon]2 allele on diseases in the elderly and survival remains elusive. We aggregated data of 38,537 individuals of European ancestry (mean age 65.5 years; 55.6% women) from six population-based cohort studies (Rotterdam Study, AGES-Reykjavik Study, Cardiovascular Health Study, Health-ABC Study, and the family-based Framingham Heart Study and Long Life Family Study) to determine the association of APOE, and in particular APOE-[epsilon]2, with survival in the population. During a mean follow-up of 11.7 years, 17,021 individuals died. Compared with homozygous APOE-[epsilon]3 carriers, APOE-[epsilon]2 carriers were at lower risk of death (hazard ratio,95% confidence interval: 0.94,0.90-0.99; P = 1.1*10.sup.-2 ), whereas APOE-[epsilon]4 carriers were at increased risk of death (HR 1.17,1.12-1.21; P = 2.8*10.sup.-16). APOE was associated with mortality risk in a dose-dependent manner, with risk estimates lowest for homozygous APOE-[epsilon]2 (HR 0.89,0.74-1.08), and highest for homozygous APOE-[epsilon]4 (HR 1.52,1.37-1.70). After censoring for dementia, effect estimates remained similar for APOE-[epsilon]2 (HR 0.95,0.90-1.01), but attenuated for APOE-[epsilon]4 (HR 1.07,1.01-1.12). Results were broadly similar across cohorts, and did not differ by age or sex. APOE genotype was associated with baseline lipid fractions (e.g. mean difference(95%CI) in LDL(mg/dL) for [epsilon]2 versus [epsilon]33: -17.1(-18.1-16.0), and [epsilon]4 versus [epsilon]33: +5.7(4.8;6.5)), but the association between APOE and mortality was unaltered after adjustment for baseline LDL or cardiovascular disease. Given the European ancestry of the study population, results may not apply to other ethnicities. Compared with APOE-[epsilon]3, APOE-[epsilon]2 is associated with prolonged survival, whereas mortality risk is increased for APOE-[epsilon]4 carriers. Further collaborative efforts are needed to unravel the role of APOE and in particular APOE-[epsilon]2 in health and disease. Apolipoprotein E is a glycoprotein best known as a mediator and regulator of lipid transport and uptake. The APOE-ε4 allele has long been associated with increased risks of Alzheimer's disease and mortality, but the effect of the less prevalent APOE-ε2 allele on diseases in the elderly and survival remains elusive. We aggregated data of 38,537 individuals of European ancestry (mean age 65.5 years; 55.6% women) from six population-based cohort studies (Rotterdam Study, AGES-Reykjavik Study, Cardiovascular Health Study, Health-ABC Study, and the family-based Framingham Heart Study and Long Life Family Study) to determine the association of APOE, and in particular APOE-ε2, with survival in the population. During a mean follow-up of 11.7 years, 17,021 individuals died. Compared with homozygous APOE-ε3 carriers, APOE-ε2 carriers were at lower risk of death (hazard ratio,95% confidence interval: 0.94,0.90-0.99; P = 1.1*10-2), whereas APOE-ε4 carriers were at increased risk of death (HR 1.17,1.12-1.21; P = 2.8*10-16). APOE was associated with mortality risk in a dose-dependent manner, with risk estimates lowest for homozygous APOE-ε2 (HR 0.89,0.74-1.08), and highest for homozygous APOE-ε4 (HR 1.52,1.37-1.70). After censoring for dementia, effect estimates remained similar for APOE-ε2 (HR 0.95,0.90-1.01), but attenuated for APOE-ε4 (HR 1.07,1.01-1.12). Results were broadly similar across cohorts, and did not differ by age or sex. APOE genotype was associated with baseline lipid fractions (e.g. mean difference(95%CI) in LDL(mg/dL) for ε2 versus ε33: -17.1(-18.1-16.0), and ε4 versus ε33: +5.7(4.8;6.5)), but the association between APOE and mortality was unaltered after adjustment for baseline LDL or cardiovascular disease. Given the European ancestry of the study population, results may not apply to other ethnicities. Compared with APOE-ε3, APOE-ε2 is associated with prolonged survival, whereas mortality risk is increased for APOE-ε4 carriers. Further collaborative efforts are needed to unravel the role of APOE and in particular APOE-ε2 in health and disease. Apolipoprotein E is a glycoprotein best known as a mediator and regulator of lipid transport and uptake. The APOE-ε4 allele has long been associated with increased risks of Alzheimer's disease and mortality, but the effect of the less prevalent APOE-ε2 allele on diseases in the elderly and survival remains elusive.BACKGROUNDApolipoprotein E is a glycoprotein best known as a mediator and regulator of lipid transport and uptake. The APOE-ε4 allele has long been associated with increased risks of Alzheimer's disease and mortality, but the effect of the less prevalent APOE-ε2 allele on diseases in the elderly and survival remains elusive.We aggregated data of 38,537 individuals of European ancestry (mean age 65.5 years; 55.6% women) from six population-based cohort studies (Rotterdam Study, AGES-Reykjavik Study, Cardiovascular Health Study, Health-ABC Study, and the family-based Framingham Heart Study and Long Life Family Study) to determine the association of APOE, and in particular APOE-ε2, with survival in the population.METHODSWe aggregated data of 38,537 individuals of European ancestry (mean age 65.5 years; 55.6% women) from six population-based cohort studies (Rotterdam Study, AGES-Reykjavik Study, Cardiovascular Health Study, Health-ABC Study, and the family-based Framingham Heart Study and Long Life Family Study) to determine the association of APOE, and in particular APOE-ε2, with survival in the population.During a mean follow-up of 11.7 years, 17,021 individuals died. Compared with homozygous APOE-ε3 carriers, APOE-ε2 carriers were at lower risk of death (hazard ratio,95% confidence interval: 0.94,0.90-0.99; P = 1.1*10-2), whereas APOE-ε4 carriers were at increased risk of death (HR 1.17,1.12-1.21; P = 2.8*10-16). APOE was associated with mortality risk in a dose-dependent manner, with risk estimates lowest for homozygous APOE-ε2 (HR 0.89,0.74-1.08), and highest for homozygous APOE-ε4 (HR 1.52,1.37-1.70). After censoring for dementia, effect estimates remained similar for APOE-ε2 (HR 0.95,0.90-1.01), but attenuated for APOE-ε4 (HR 1.07,1.01-1.12). Results were broadly similar across cohorts, and did not differ by age or sex. APOE genotype was associated with baseline lipid fractions (e.g. mean difference(95%CI) in LDL(mg/dL) for ε2 versus ε33: -17.1(-18.1-16.0), and ε4 versus ε33: +5.7(4.8;6.5)), but the association between APOE and mortality was unaltered after adjustment for baseline LDL or cardiovascular disease. Given the European ancestry of the study population, results may not apply to other ethnicities.RESULTSDuring a mean follow-up of 11.7 years, 17,021 individuals died. Compared with homozygous APOE-ε3 carriers, APOE-ε2 carriers were at lower risk of death (hazard ratio,95% confidence interval: 0.94,0.90-0.99; P = 1.1*10-2), whereas APOE-ε4 carriers were at increased risk of death (HR 1.17,1.12-1.21; P = 2.8*10-16). APOE was associated with mortality risk in a dose-dependent manner, with risk estimates lowest for homozygous APOE-ε2 (HR 0.89,0.74-1.08), and highest for homozygous APOE-ε4 (HR 1.52,1.37-1.70). After censoring for dementia, effect estimates remained similar for APOE-ε2 (HR 0.95,0.90-1.01), but attenuated for APOE-ε4 (HR 1.07,1.01-1.12). Results were broadly similar across cohorts, and did not differ by age or sex. APOE genotype was associated with baseline lipid fractions (e.g. mean difference(95%CI) in LDL(mg/dL) for ε2 versus ε33: -17.1(-18.1-16.0), and ε4 versus ε33: +5.7(4.8;6.5)), but the association between APOE and mortality was unaltered after adjustment for baseline LDL or cardiovascular disease. Given the European ancestry of the study population, results may not apply to other ethnicities.Compared with APOE-ε3, APOE-ε2 is associated with prolonged survival, whereas mortality risk is increased for APOE-ε4 carriers. Further collaborative efforts are needed to unravel the role of APOE and in particular APOE-ε2 in health and disease.CONCLUSIONCompared with APOE-ε3, APOE-ε2 is associated with prolonged survival, whereas mortality risk is increased for APOE-ε4 carriers. Further collaborative efforts are needed to unravel the role of APOE and in particular APOE-ε2 in health and disease. Background Apolipoprotein E is a glycoprotein best known as a mediator and regulator of lipid transport and uptake. The APOE-ε4 allele has long been associated with increased risks of Alzheimer's disease and mortality, but the effect of the less prevalent APOE-ε2 allele on diseases in the elderly and survival remains elusive. Methods We aggregated data of 38,537 individuals of European ancestry (mean age 65.5 years; 55.6% women) from six population-based cohort studies (Rotterdam Study, AGES-Reykjavik Study, Cardiovascular Health Study, Health-ABC Study, and the family-based Framingham Heart Study and Long Life Family Study) to determine the association of APOE, and in particular APOE-ε2, with survival in the population. Results During a mean follow-up of 11.7 years, 17,021 individuals died. Compared with homozygous APOE-ε3 carriers, APOE-ε2 carriers were at lower risk of death (hazard ratio,95% confidence interval: 0.94,0.90–0.99; P = 1.1*10−2), whereas APOE-ε4 carriers were at increased risk of death (HR 1.17,1.12–1.21; P = 2.8*10−16). APOE was associated with mortality risk in a dose-dependent manner, with risk estimates lowest for homozygous APOE-ε2 (HR 0.89,0.74–1.08), and highest for homozygous APOE-ε4 (HR 1.52,1.37–1.70). After censoring for dementia, effect estimates remained similar for APOE-ε2 (HR 0.95,0.90–1.01), but attenuated for APOE-ε4 (HR 1.07,1.01–1.12). Results were broadly similar across cohorts, and did not differ by age or sex. APOE genotype was associated with baseline lipid fractions (e.g. mean difference(95%CI) in LDL(mg/dL) for ε2 versus ε33: -17.1(-18.1–16.0), and ε4 versus ε33: +5.7(4.8;6.5)), but the association between APOE and mortality was unaltered after adjustment for baseline LDL or cardiovascular disease. Given the European ancestry of the study population, results may not apply to other ethnicities. Conclusion Compared with APOE-ε3, APOE-ε2 is associated with prolonged survival, whereas mortality risk is increased for APOE-ε4 carriers. Further collaborative efforts are needed to unravel the role of APOE and in particular APOE-ε2 in health and disease. Background Apolipoprotein E is a glycoprotein best known as a mediator and regulator of lipid transport and uptake. The APOE-ε4 allele has long been associated with increased risks of Alzheimer's disease and mortality, but the effect of the less prevalent APOE-ε2 allele on diseases in the elderly and survival remains elusive. Methods We aggregated data of 38,537 individuals of European ancestry (mean age 65.5 years; 55.6% women) from six population-based cohort studies (Rotterdam Study, AGES-Reykjavik Study, Cardiovascular Health Study, Health-ABC Study, and the family-based Framingham Heart Study and Long Life Family Study) to determine the association of APOE, and in particular APOE-ε2, with survival in the population. Results During a mean follow-up of 11.7 years, 17,021 individuals died. Compared with homozygous APOE-ε3 carriers, APOE-ε2 carriers were at lower risk of death (hazard ratio,95% confidence interval: 0.94,0.90–0.99; P = 1.1*10−2), whereas APOE-ε4 carriers were at increased risk of death (HR 1.17,1.12–1.21; P = 2.8*10−16). APOE was associated with mortality risk in a dose-dependent manner, with risk estimates lowest for homozygous APOE-ε2 (HR 0.89,0.74–1.08), and highest for homozygous APOE-ε4 (HR 1.52,1.37–1.70). After censoring for dementia, effect estimates remained similar for APOE-ε2 (HR 0.95,0.90–1.01), but attenuated for APOE-ε4 (HR 1.07,1.01–1.12). Results were broadly similar across cohorts, and did not differ by age or sex. APOE genotype was associated with baseline lipid fractions (e.g. mean difference(95%CI) in LDL(mg/dL) for ε2 versus ε33: -17.1(-18.1–16.0), and ε4 versus ε33: +5.7(4.8;6.5)), but the association between APOE and mortality was unaltered after adjustment for baseline LDL or cardiovascular disease. Given the European ancestry of the study population, results may not apply to other ethnicities. Conclusion Compared with APOE-ε3, APOE-ε2 is associated with prolonged survival, whereas mortality risk is increased for APOE-ε4 carriers. Further collaborative efforts are needed to unravel the role of APOE and in particular APOE-ε2 in health and disease. BackgroundApolipoprotein E is a glycoprotein best known as a mediator and regulator of lipid transport and uptake. The APOE-ε4 allele has long been associated with increased risks of Alzheimer's disease and mortality, but the effect of the less prevalent APOE-ε2 allele on diseases in the elderly and survival remains elusive.MethodsWe aggregated data of 38,537 individuals of European ancestry (mean age 65.5 years; 55.6% women) from six population-based cohort studies (Rotterdam Study, AGES-Reykjavik Study, Cardiovascular Health Study, Health-ABC Study, and the family-based Framingham Heart Study and Long Life Family Study) to determine the association of APOE, and in particular APOE-ε2, with survival in the population.ResultsDuring a mean follow-up of 11.7 years, 17,021 individuals died. Compared with homozygous APOE-ε3 carriers, APOE-ε2 carriers were at lower risk of death (hazard ratio,95% confidence interval: 0.94,0.90-0.99; P = 1.1*10-2), whereas APOE-ε4 carriers were at increased risk of death (HR 1.17,1.12-1.21; P = 2.8*10-16). APOE was associated with mortality risk in a dose-dependent manner, with risk estimates lowest for homozygous APOE-ε2 (HR 0.89,0.74-1.08), and highest for homozygous APOE-ε4 (HR 1.52,1.37-1.70). After censoring for dementia, effect estimates remained similar for APOE-ε2 (HR 0.95,0.90-1.01), but attenuated for APOE-ε4 (HR 1.07,1.01-1.12). Results were broadly similar across cohorts, and did not differ by age or sex. APOE genotype was associated with baseline lipid fractions (e.g. mean difference(95%CI) in LDL(mg/dL) for ε2 versus ε33: -17.1(-18.1-16.0), and ε4 versus ε33: +5.7(4.8;6.5)), but the association between APOE and mortality was unaltered after adjustment for baseline LDL or cardiovascular disease. Given the European ancestry of the study population, results may not apply to other ethnicities.ConclusionCompared with APOE-ε3, APOE-ε2 is associated with prolonged survival, whereas mortality risk is increased for APOE-ε4 carriers. Further collaborative efforts are needed to unravel the role of APOE and in particular APOE-ε2 in health and disease. |
| Audience | Academic |
| Author | Vasan, Ramachandran S. Zilhao, Nuno R. Ghanbari, Mohsen Li, Shuo Bis, Joshua C. Kulminski, Alexander M. Launer, Lenore Psaty, Bruce M. Ikram, M. Arfan Tranah, Gregory J. Seshadri, Sudha Gudnason, Vilmundur Yang, Qiong Wolters, Frank J. Biggs, Mary L. Harris, Tamara B. Jakobsdottir, Johanna Evans, Daniel S. |
| AuthorAffiliation | 5 Faculty of Medicine, University of Iceland, Reykavik, Iceland 7 Laboratory of Epidemiology, Demography, and Biometry, National Institute on Aging, Bethesda, Maryland, United States of America 3 Cardiovascular Health Research Unit, Department of Medicine, University of Washington, Seattle, Washington, United States of America 1 Department of Epidemiology, Erasmus Medical Centre, Rotterdam, the Netherlands 6 California Pacific Medical Center Research Institute, San Francisco, California, United States of America 10 Departments of Epidemiology and Health Services, University of Washington, Seattle, Washington, United States of America 2 Department of Biostatistics, Boston University School of Public Health, Boston, Massachusetts, United States of America 11 Kaiser Permanente Washington Health Research Institute, Seattle, Washington, United States of America 12 Biodemography of Aging Research Unit, Social Science Research Institute, Duke University, Durham, North Carolina, United States of Ameri |
| AuthorAffiliation_xml | – name: 3 Cardiovascular Health Research Unit, Department of Medicine, University of Washington, Seattle, Washington, United States of America – name: 8 Sections of Preventive Medicine and Epidemiology, and Cardiology, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, United States of America – name: 7 Laboratory of Epidemiology, Demography, and Biometry, National Institute on Aging, Bethesda, Maryland, United States of America – name: 4 Department of Biostatistics, University of Washington, Seattle, Washington, United States of America – name: Nathan S Kline Institute, UNITED STATES – name: 1 Department of Epidemiology, Erasmus Medical Centre, Rotterdam, the Netherlands – name: 11 Kaiser Permanente Washington Health Research Institute, Seattle, Washington, United States of America – name: 5 Faculty of Medicine, University of Iceland, Reykavik, Iceland – name: 6 California Pacific Medical Center Research Institute, San Francisco, California, United States of America – name: 10 Departments of Epidemiology and Health Services, University of Washington, Seattle, Washington, United States of America – name: 2 Department of Biostatistics, Boston University School of Public Health, Boston, Massachusetts, United States of America – name: 12 Biodemography of Aging Research Unit, Social Science Research Institute, Duke University, Durham, North Carolina, United States of America – name: 9 Icelandic Heart Association, Kopavogur, Iceland – name: 13 Department of Neurology, Boston University School of Medicine, Boston, Massachusetts, United States of America |
| Author_xml | – sequence: 1 givenname: Frank J. orcidid: 0000-0003-2226-4050 surname: Wolters fullname: Wolters, Frank J. – sequence: 2 givenname: Qiong surname: Yang fullname: Yang, Qiong – sequence: 3 givenname: Mary L. surname: Biggs fullname: Biggs, Mary L. – sequence: 4 givenname: Johanna surname: Jakobsdottir fullname: Jakobsdottir, Johanna – sequence: 5 givenname: Shuo orcidid: 0000-0003-2331-2448 surname: Li fullname: Li, Shuo – sequence: 6 givenname: Daniel S. surname: Evans fullname: Evans, Daniel S. – sequence: 7 givenname: Joshua C. surname: Bis fullname: Bis, Joshua C. – sequence: 8 givenname: Tamara B. surname: Harris fullname: Harris, Tamara B. – sequence: 9 givenname: Ramachandran S. surname: Vasan fullname: Vasan, Ramachandran S. – sequence: 10 givenname: Nuno R. surname: Zilhao fullname: Zilhao, Nuno R. – sequence: 11 givenname: Mohsen surname: Ghanbari fullname: Ghanbari, Mohsen – sequence: 12 givenname: M. Arfan surname: Ikram fullname: Ikram, M. Arfan – sequence: 13 givenname: Lenore surname: Launer fullname: Launer, Lenore – sequence: 14 givenname: Bruce M. surname: Psaty fullname: Psaty, Bruce M. – sequence: 15 givenname: Gregory J. surname: Tranah fullname: Tranah, Gregory J. – sequence: 16 givenname: Alexander M. surname: Kulminski fullname: Kulminski, Alexander M. – sequence: 17 givenname: Vilmundur surname: Gudnason fullname: Gudnason, Vilmundur – sequence: 18 givenname: Sudha surname: Seshadri fullname: Seshadri, Sudha |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31356640$$D View this record in MEDLINE/PubMed |
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| Snippet | Apolipoprotein E is a glycoprotein best known as a mediator and regulator of lipid transport and uptake. The APOE-ε4 allele has long been associated with... Background Apolipoprotein E is a glycoprotein best known as a mediator and regulator of lipid transport and uptake. The APOE-[epsilon]4 allele has long been... Apolipoprotein E is a glycoprotein best known as a mediator and regulator of lipid transport and uptake. The APOE-[epsilon]4 allele has long been associated... Background Apolipoprotein E is a glycoprotein best known as a mediator and regulator of lipid transport and uptake. The APOE-ε4 allele has long been associated... BackgroundApolipoprotein E is a glycoprotein best known as a mediator and regulator of lipid transport and uptake. The APOE-ε4 allele has long been associated... Background Apolipoprotein E is a glycoprotein best known as a mediator and regulator of lipid transport and uptake. The APOE-ε4 allele has long been associated... |
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| SubjectTerms | Age Aged Aging Alleles Alzheimer's disease Apolipoprotein E Apolipoproteins Apolipoproteins E - genetics Biology and Life Sciences Biometrics Cancer Cardiovascular diseases Carriers Cohort analysis Cohort Studies Confidence intervals Dementia disorders Demography Disease Epidemiology Family studies Female Genomes Genotype Genotype & phenotype Genotypes Geriatrics Glycoproteins Health care Health risks Heart Heterozygote Humans Laboratories Lipids Lipids - blood Low density lipoprotein Male Medical research Medicine and Health Sciences Meta-analysis Meta-Analysis as Topic Mortality Mortality risk Neurodegenerative diseases Patient outcomes People and Places Population Population studies Population-based studies Preventive medicine Public health Research and Analysis Methods Risk Risk factors Studies Survival Survival Analysis Systematic review |
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| Title | The impact of APOE genotype on survival: Results of 38,537 participants from six population-based cohorts (E2-CHARGE) |
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