The DOI matches its Crossref record; 58 of the 59 references it cites were found in a registry or an index.
Apolipoprotein E alleles, dyslipidemia, and coronary heart disease. The Framingham Offspring Study
Abstract
Objective To describe the association between apolipoprotein E alleles (epsilon 2, epsilon 3, and epsilon 4), dyslipidemias, and coronary heart disease (CHD). Design Cross-sectional prevalence study. Setting and participants Community-based sample of men (n = 1034) and women (n = 916) aged 40 to 77 years who are participating in a long-term study of cardiovascular disease. Study participants underwent fasting lipid measurements, coronary risk factor determinations, and a comprehensive evaluation for the presence of current or previous CHD. Results Compared with the epsilon 3 allele, the epsilon 4 allele was associated with elevated low-density lipoprotein cholesterol values (> or = 4.14 mmol/L [160 mg/dL]) in women, the epsilon 2 and epsilon 4 alleles were associated with moderately elevated triglyceride values (> or = 2.82 mmol/L [250 mg/dL]) in men, and the epsilon 2 allele was associated with severely elevated triglyceride values (> or = 5.64 mmol/L [500 mg/dL]) in men. The apolipoprotein E alleles were not associated with hypertension, obesity, smoking, or diabetes, but the epsilon 4 allele frequency was reduced in women after 60 years of age. The age-adjusted prevalence of CHD was associated with the epsilon 4 allele in both men (relative odds = 1.53, P = .04) and women (relative odds = 1.99, P = .05). In analyses for women and for both sexes combined, this relation persisted after adjustment by hypertension, smoking, obesity, diabetes, high-density lipoprotein cholester…
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“The apoE4 isoform has been linked with increased levels of LDL and has been demonstrated to be a risk factor for cardiovascular disease (Song et al., 2004; Wilson et al., 1994).”
From The role of apolipoprotein E in Alzheimer's disease (2009) · cites this paper as Wilson et al., 1994
In the citing paper
“a decreased risk of coronary artery disease (unless it is associated with type III hyperlipoproteinemia), 42,43”
From Preclinical Evidence of Alzheimer's Disease in Persons Homozygous for the ε4 Allele for Apolipoprotein E (1996) · cites this paper as [43]
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Friedewald, W. T., Levy, R. I., & Fredrickson, D. S. (1972) · Clinical Chemistry · doi:10.1093/clinchem/18.6.499 · Cited by 32,423
Grundy, S. M., Bilheimer, D. W., Chait, A., Clark, L. T., Denke, M. A., Havel, R. J., Hazzard, W. R., Hulley, S. B., Hunninghake, D. B., Kreisberg, R. A., et al. (1993) · JAMA · doi:10.1001/jama.269.23.3015 · Cited by 27,944
Corder, E. H., Saunders, A. M., Strittmatter, W. J., Schmechel, D. E., Gaskell, P. C., Small, G. W., Roses, A. D., Haines, J. L., & Pericak-Vance, M. A. (1993) · Science · doi:10.1126/science.8346443 · Cited by 9,429
A Receptor-Mediated Pathway for Cholesterol Homeostasis
Brown, M. S., & Goldstein, J. L. (1986) · Science · doi:10.1126/science.3513311 · Cited by 5,703
Strittmatter, W. J., Saunders, A. M., Schmechel, D., Pericak-Vance, M., Enghild, J., Salvesen, G. S., & Roses, A. D. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.5.1977 · Cited by 4,268
Association of apolipoprotein E allele ϵ4 with late‐onset familial and sporadic Alzheimer's disease
Saunders, A. M., Strittmatter, W. J., Schmechel, D., St. George-Hyslop, P. H., Pericak-Vance, M. A., Joo, S. H., Rosi, B. L., Gusella, J. F., Crapper-MacLachlan, D. R., Alberts, M. J., et al. (1993) · Neurology · doi:10.1212/wnl.43.8.1467 · Cited by 3,786
Warnick, G. R., Benderson, J., & Albers, J. J. (1982) · Clinical Chemistry · doi:10.1093/clinchem/28.6.1379 · Cited by 2,154
Apolipoprotein E polymorphism and atherosclerosis.
Davignon, J., Gregg, R. E., & Sing, C. F. (1988) · Arteriosclerosis: An Official Journal of the American Heart Association, Inc. · doi:10.1161/01.atv.8.1.1 · Cited by 1,981
Schmechel, D. E., Saunders, A. M., Strittmatter, W. J., Crain, B. J., Hulette, C. M., Joo, S. H., Pericak-Vance, M. A., Goldgaber, D., & Roses, A. D. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.20.9649 · Cited by 1,525
Strittmatter, W. J., Weisgraber, K. H., Huang, D. Y., Dong, L. M., Salvesen, G. S., Pericak-Vance, M., Schmechel, D., Saunders, A. M., Goldgaber, D., & Roses, A. D. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.17.8098 · Cited by 1,363
Cited by
Sorted by citations
A Quantitative Assessment of Plasma Homocysteine as a Risk Factor for Vascular Disease
Boushey, C. J. (1995) · JAMA · doi:10.1001/jama.1995.03530130055028 · Cited by 3,708
The role of apolipoprotein E in Alzheimer's disease
Kim, J., Basak, J. M., & Holtzman, D. M. (2009) · Neuron · doi:10.1016/j.neuron.2009.06.026 · Cited by 1,661
Distinct patterns of brain activity in young carriers of the APOE -ε4 allele
Filippini, N., MacIntosh, B. J., Hough, M. G., Goodwin, G. M., Frisoni, G. B., Smith, S. M., Matthews, P. M., Beckmann, C. F., & Mackay, C. E. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0811879106 · Cited by 1,613
Reiman, E. M., Caselli, R. J., Yun, L. S., Chen, K., Bandy, D., Minoshima, S., Thibodeau, S. N., & Osborne, D. (1996) · New England Journal of Medicine · doi:10.1056/nejm199603213341202 · Cited by 1,366
Genetic analysis of ageing: role of oxidative damage and environmental stresses
Martin, G. M., Austad, S. N., & Johnson, T. E. (1996) · Nature Genetics · doi:10.1038/ng0596-25 · Cited by 646
Metadata
- Authors
- Wilson, P. W. F.
- Corresponding author
- Wilson, Peter W. F.
- ORCID
- Wilson, Peter W. F.
- Venue
- JAMA
- Publisher
- American Medical Association (AMA)
- Published
- 1994-12-07
- Volume
- 272
- Issue
- 21
- Pages
- 1666
- ISSN
- 0002-9955 (ISSN-L)
- 0098-7484
- OpenAlex
- W4237709179
- Cited by
- 468
- References
- 59
- Citations by year
- 2025: 1 · 2024: 3 · 2023: 10 · 2022: 3 · 2021: 5 · 2020: 6 · 2019: 4 · 2018: 2 · 2017: 6 · 2016: 7 · 2015: 7 · 2014: 7 · 2013: 14 · 2012: 9
- FWCI
- 21.68
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- JAMA (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- apolipoprotein E, apolipoprotein E ε4 allele, dyslipidemia, coronary artery disease, LDL cholesterol, triglycerides, sex differences, genetic risk factors, Framingham Offspring Study
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