HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Correspondence: Submit a response Alert me when this article is cited Alert me when Correspondence are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wang, J. C. Articles by Goate, A. Search for Related Content PubMed PubMed Citation Articles by Wang, J. C. Articles by Goate, A.

Effect of APOE genotype and promoter polymorphism on risk of Alzheimer’s disease

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.

Address correspondence and reprint requests to Dr. Alison Goate, Department of Psychiatry, Box 8134, Washington University School of Medicine, St. Louis, MO 63110; e-mail: goatea{at}psychiatry.wustl.edu

Article 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 4 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 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.

This article has been cited by other articles:

				C. W. Hogue, R. Fucetola, T. Hershey, K. Freedland, V. G. Davila-Roman, A. M. Goate, and R. E. Thompson Risk factors for neurocognitive dysfunction after cardiac surgery in postmenopausal women. Ann. Thorac. Surg., August 1, 2008; 86(2): 511 - 516. [Abstract] [Full Text] [PDF]

				O. Belbin, J. L. Dunn, Y. Ling, L. Morgan, S. Chappell, H. Beaumont, D. Warden, D. A. Smith, N. Kalsheker, and K. Morgan Regulatory region single nucleotide polymorphisms of the apolipoprotein E gene and the rate of cognitive decline in Alzheimer's disease Hum. Mol. Genet., September 15, 2007; 16(18): 2199 - 2208. [Abstract] [Full Text] [PDF]

				J-C Lambert, N Coyle, and C Lendon The allelic modulation of apolipoprotein E expression by oestrogen: potential relevance for Alzheimer's disease J. Med. Genet., February 1, 2004; 41(2): 104 - 112. [Abstract] [Full Text] [PDF]

				F. M. Harris, I. Tesseur, W. J. Brecht, Q. Xu, K. Mullendorff, S. Chang, T. Wyss-Coray, R. W. Mahley, and Y. Huang Astroglial Regulation of Apolipoprotein E Expression in Neuronal Cells: IMPLICATIONS FOR ALZHEIMER'S DISEASE J. Biol. Chem., January 30, 2004; 279(5): 3862 - 3868. [Abstract] [Full Text] [PDF]

				J. C. Lambert, L. Araria-Goumidi, L. Myllykangas, C. Ellis, J. C. Wang, M. J. Bullido, J. M. Harris, M. J. Artiga, D. Hernandez, J. M. Kwon, et al. Contribution of APOE promoter polymorphisms to Alzheimer's disease risk Neurology, July 9, 2002; 59(1): 59 - 66. [Abstract] [Full Text] [PDF]