|
|
||||||||
From the Department of Epidemiology and Biostatistics (Drs. Drigalenko and Elston), Rammelkamp Center for Education and Research, MetroHealth Campus, Case Western Reserve University, Cleveland, OH; and the Department of Neurology (Dr. Poduslo), Texas Tech University Health Sciences Center, Lubbock, TX.
Address correspondence and reprint requests to Dr. Robert Elston, Department of Epidemiology and Biostatistics, Rammelkamp Center for Education and Research, MetroHealth Campus, Case Western Reserve University, 2500 MetroHealth Drive, Room R259, Cleveland, OH 44109-1998.
Objective: The association between Alzheimer's disease (AD) and alleles at the ApoE and the ApoCI loci were tested.
Background: The ApoE alleles, in linkage disequlibrium with ApoCI alleles, have been reported as associated with (
4) or protective for (
2) AD.
Methods: The patients comprise two samples, with a total of 176 whose diagnosis has been confirmed as having probable AD and 226 controls. Genomic DNA was extracted from blood or transformed lymphocytes. Logistic regression was used to determine the effects of alleles at the ApoE and ApoCI loci after allowing for the effects of age and gender.
Results: The effects of the ApoE
2,
3, and
4 alleles were individually studied first; ignoring the ApoCI locus, only the dominant or additive effect of
4 is significant after considering age, gender, and sample-the dominant effect being slightly more significant. The effect of
4 (when only the ApoE locus is included in the model) was larger than recently reported: the odds ratio was 5.57 (95% CI, 3.46 to 8.98). Similarly, when the ApoCI locus was examined, ignoring the ApoE locus, a dominant effect of A was found to be slightly more significant than an additive effect. Finally, models were considered that included the dominant effect of
4, the dominant effect of A, and their interaction. A model that included only the interaction of ApoE and ApoCI yielded the largest odds ratio, 5.89 (95% CI, 3.64 to 9.53).
Conclusions: Association of AD with both the ApoE
4 and ApoCI A alleles was found. The increased risk of AD among carriers of
4 was found to be higher among those who also bear the ApoCI A allele but this may be due to a dose effect of the
4 allele.
Supported in part by research grant F05 TW05285 from the Fogarty International Center, U.S. Public Health Service resource grant P41 RR03655 from the National Center for Research Resources and research grant GM 28356 from the National Institute of General Medical Sciences, and funds from the state of Texas.
Received August 1, 1997. Accepted in final form March 5, 1998.
This article has been cited by other articles:
![]() |
K. Abildayeva, J. F. P. Berbee, A. Blokland, P. J. Jansen, F. J. Hoek, O. Meijer, D. Lutjohann, T. Gautier, T. Pillot, J. De Vente, et al. Human apolipoprotein C-I expression in mice impairs learning and memory functions J. Lipid Res., April 1, 2008; 49(4): 856 - 869. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. Tycko, J. H. Lee, A. Ciappa, A. Saxena, C.-M. Li, L. Feng, A. Arriaga, Y. Stern, R. Lantigua, N. Shachter, et al. APOE and APOC1 Promoter Polymorphisms and the Risk of Alzheimer Disease in African American and Caribbean Hispanic Individuals Arch Neurol, September 1, 2004; 61(9): 1434 - 1439. [Abstract] [Full Text] [PDF] |
||||
![]() |
Other articles noted Evid. Based Ment. Health, February 1, 1999; 2(1): 8 - 8. [Full Text] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |