The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Effect of APOE genotype and promoter polymorphism on risk of Alzheimer’s disease
Abstract
Objective To verify the association between APOE gene promoter polymorphisms and the development of AD and to determine whether the effect of promoter polymorphisms on AD is independent of the APOE epsilon4 allele. Background Three polymorphisms in the APOE promoter have been shown to modify APOE expression in vitro. Several studies have suggested that these polymorphisms may also modulate risk for AD, either independently or by modifying the effect of the APOE coding polymorphism. Methods The authors analyzed allele and genotype distributions for APOE and all three known APOE promoter polymorphisms (-491 A/T, -427 T/C, and -219 G/T) in a study group consisting of 237 subjects with AD and 274 age-matched controls. They then used log-linear and logistic regression analyses to test for possible interactions between APOE genotype and the promoter polymorphisms on risk of AD. Conclusion A strong association between the APOE epsilon 4 allele and AD was detected regardless of promoter polymorphism status. In addition, the -491 AA genotype appears to be an independent genetic risk factor for AD. The -427 T/C polymorphism and the -219 T/G polymorphism were not directly associated with AD.
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“The apolipoprotein E4 (APOE4) allele is the most common and important genetic risk factor for late-onset sporadic AD [19–21].”
From 25-Hydroxycholesterol amplifies microglial IL-1β production in an apoE isoform-dependent manner (2020) · cites this paper as [21]
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Protective effect of apolipoprotein E type 2 allele for late onset Alzheimer disease
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Lack of apolipoprotein E dramatically reduces amyloid β-peptide deposition
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Allelic polymorphisms in the transcriptional regulatory region of apolipoprotein E gene
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Cited by
Sorted by citations
Apolipoprotein Eε4 modifies Alzheimer's disease onset in an E280A PS1 kindred
Pastor, P., Roe, C. M., Villegas, A., Bedoya, G., Chakraverty, S., García, G., Tirado, V., Norton, J., Ríos, S., Martínez, M., et al. (2003) · Annals of Neurology · doi:10.1002/ana.10636 · Cited by 194
Self-citation25-Hydroxycholesterol amplifies microglial IL-1β production in an apoE isoform-dependent manner
Wong, M. Y., Lewis, M., Doherty, J. J., Shi, Y., Cashikar, A. G., Amelianchik, A., Tymchuk, S., Sullivan, P. M., Qian, M., Covey, D. F., et al. (2020) · Journal of Neuroinflammation · doi:10.1186/s12974-020-01869-3 · Cited by 121
Choi, K., Lee, J., Gunasekaran, T., Kang, S., Lee, W., Jeong, J., Lim, H., Zhang, X., Zhu, C., Won, S.-Y., et al. (2019) · Journal of Clinical Medicine · doi:10.3390/jcm8081236 · Cited by 72
Maloney, B., Ge, Y., Alley, G. M., & Lahiri, D. K. (2007) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2007.04831.x · Cited by 63
Metadata
- Authors
- Wang, J. C., Kwon, J. M., Shah, P., Morris, J. C., & Goate, A.
- Affiliations
- From the Departments of Psychiatry (Drs. Wang and Goate), Neurology (Drs. Kwon and Morris), Biology (P. Shah), and Genetics (Dr. Goate), Washington University School of Medicine, St. Louis, MO.
- Venue
- Neurology
- Published
- 2000-12-12
- Volume
- 55
- Issue
- 11
- Pages
- 1644-1649
- ISSN
- 0028-3878
- 1526-632X
- Cited by
- 49
- References
- 5
- Language
- en
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