Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (94)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Artiga, M. J.
Right arrow Articles by Valdivieso, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Artiga, M. J.
Right arrow Articles by Valdivieso, F.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Human Molecular Genetics, Vol 7, 1887-1892, Copyright © 1998 by Oxford University Press

ARTICLES

Risk for Alzheimer's disease correlates with transcriptional activity of the APOE gene

MJ Artiga, MJ Bullido, A Frank, I Sastre, M Recuero, MA Garcia, CL Lendon, SW Han, JC Morris, J Vazquez, A Goate and F Valdivieso
Departamento de Biologia Molecular and Centro de Biologia Molecular Severo Ochoa (CSIC-UAM), 28049 Madrid, Spain.

While the straightepsilon4 allele of apolipoprotein E ( APOE, gene; ApoE, protein) is widely accepted as a major genetic risk factor for the late onset form of Alzheimer's disease (AD), recent evidence points to variations in ApoE levels as another important factor. We have previously reported that a common variant in the regulatory region of APOE (-491A) is associated with risk for late onset AD. In this report we analyze the association of another APOE promoter polymorphism (- 427T/C) with AD in two case-control clinical samples and demonstrate a correlation between APOE promoter transcriptional activity and risk for AD. The association studies show that the allelic variant (-427C) and the haplotype [-491A-427C] of the APOE promoter are associated with increased risk for AD. Study of the transcriptional activity of the common haplotypes defined by combination of the -491 and -427 alleles indicated that the risk for late onset AD positively correlates with transcriptional activity of the APOE gene, suggesting that increases in the local expression of ApoE could be responsible for the association of APOE promoter polymorphism with AD.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 NeurologyHome page
J. Shi, C. B. Zhao, T. L. Vollmer, T. M. Tyry, and S. M. Kuniyoshi
APOE {varepsilon}4 allele is associated with cognitive impairment in patients with multiple sclerosis
Neurology, January 15, 2008; 70(3): 185 - 190.
[Abstract] [Full Text] [PDF]

Home page
 Hum Mol GenetHome page
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]

Home page
 J. Neurosci.Home page
M. M. M. Wilhelmus, I. Otte-Holler, J. Davis, W. E. Van Nostrand, R. M. W. de Waal, and M. M. Verbeek
Apolipoprotein E Genotype Regulates Amyloid-{beta} Cytotoxicity
J. Neurosci., April 6, 2005; 25(14): 3621 - 3627.
[Abstract] [Full Text] [PDF]

Home page
 Hum Mol GenetHome page
K. M. Mann, F. E. Thorngate, Y. Katoh-Fukui, H. Hamanaka, D. L. Williams, S. Fujita, and B. T. Lamb
Independent effects of APOE on cholesterol metabolism and brain A{beta} levels in an Alzheimer disease mouse model
Hum. Mol. Genet., September 1, 2004; 13(17): 1959 - 1968.
[Abstract] [Full Text] [PDF]

Home page
 Arch NeurolHome page
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]

Home page
 J. Med. Genet.Home page
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]

Home page
 J. Biol. Chem.Home page
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]

Home page
 Nucleic Acids ResHome page
M. Campillos, J. R. Lamas, M. A. Garcia, M. J. Bullido, F. Valdivieso, and J. Vazquez
Specific interaction of heterogeneous nuclear ribonucleoprotein A1 with the -219T allelic form modulates APOE promoter activity
Nucleic Acids Res., June 15, 2003; 31(12): 3063 - 3070.
[Abstract] [Full Text] [PDF]

Home page
 Nucleic Acids ResHome page
M. Campillos, M. A. Garcia, F. Valdivieso, and J. Vazquez
Transcriptional activation by AP-2{alpha} is modulated by the oncogene DEK
Nucleic Acids Res., March 1, 2003; 31(5): 1571 - 1575.
[Abstract] [Full Text] [PDF]

Home page
 Hum Mol GenetHome page
A. B. West, D. Maraganore, J. Crook, T. Lesnick, P. J. Lockhart, K. M. Wilkes, G. Kapatos, J. A. Hardy, and M. J. Farrer
Functional association of the parkin gene promoter with idiopathic Parkinson's disease
Hum. Mol. Genet., October 15, 2002; 11(22): 2787 - 2792.
[Abstract] [Full Text] [PDF]

Home page
 NeurologyHome page
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]

Home page
 Br. J. PsychiatryHome page
C. HOLMES
Genotype and phenotype in Alzheimer's disease
The British Journal of Psychiatry, February 1, 2002; 180(2): 131 - 134.
[Abstract] [Full Text] [PDF]

Home page
 NeurologyHome page
J. C. Wang, J. M. Kwon, P. Shah, J. C. Morris, and A. Goate
Effect of APOE genotype and promoter polymorphism on risk of Alzheimer's disease
Neurology, December 12, 2000; 55(11): 1644 - 1649.
[Abstract] [Full Text] [PDF]

Home page
 Genome ResHome page
D. A. Nickerson, S. L. Taylor, S. M. Fullerton, K. M. Weiss, A. G. Clark, J. H. Stengård, V. Salomaa, E. Boerwinkle, and C. F. Sing
Sequence Diversity and Large-Scale Typing of SNPs in the Human Apolipoprotein E Gene
Genome Res., October 1, 2000; 10(10): 1532 - 1545.
[Abstract] [Full Text]

Home page
 Proc. Natl. Acad. Sci. USAHome page
K. R. Bales, T. Verina, D. J. Cummins, Y. Du, R. C. Dodel, J. Saura, C. E. Fishman, C. A. DeLong, P. Piccardo, V. Petegnief, et al.
Apolipoprotein E is essential for amyloid deposition in the APPV717F transgenic mouse model of Alzheimer's disease
PNAS, December 21, 1999; 96(26): 15233 - 15238.
[Abstract] [Full Text] [PDF]

Home page
 NeurologyHome page
V. M. Casadei, C. Ferri, F. Veglia, A. Gavazzi, G. Salani, M. Cattaneo, S. Sorbi, G. Annoni, F. Licastro, C. Mariani, et al.
APOE -491 promoter polymorphism is a risk factor for late-onset Alzheimer's disease
Neurology, November 1, 1999; 53(8): 1888 - 1888.
[Full Text]

Home page
 J. Biol. Chem.Home page
E. Salero, R. Perez-Sen, J. Aruga, C. Gimenez, and F. Zafra
Transcription Factors Zic1 and Zic2 Bind and Transactivate the Apolipoprotein E Gene Promoter
J. Biol. Chem., January 12, 2001; 276(3): 1881 - 1888.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.