Candidate single-nucleotide polymorphisms from a genomewide association study of Alzheimer disease
Abstract
OBJECTIVE: To identify single-nucleotide polymorphisms (SNPs) associated with risk and age at onset of Alzheimer disease (AD) in a genomewide association study of 469 438 SNPs. DESIGN: Case-control study with replication. SETTING: Memory referral clinics in Canada and the United Kingdom. PARTICIPANTS: The hypothesis-generating data set consisted of 753 individuals with AD by National Institute of Neurological and Communicative Diseases and Stroke/Alzheimer's Disease and Related Disorders Association criteria recruited from 9 memory referral clinics in Canada and 736 ethnically matched control subjects; control subjects were recruited from nonbiological relatives, friends, or spouses of the patients and did not exhibit cognitive impairment by history or cognitive testing. The follow-up data set consisted of 418 AD cases and 249 nondemented control cases from the United Kingdom Medical Research Council Genetic Resource for Late-Onset AD recruited from clinics at Cardiff University, Cardiff, Wales, and King's College London, London, England. MAIN OUTCOME MEASURES: Odds ratios and 95% confidence intervals for association of SNPs with AD by logistic regression adjusted for age, sex, education, study site, and French Canadian ancestry (for the Canadian data set). Hazard ratios and 95% confidence intervals from Cox proportional hazards regression for age at onset with similar covariate adjustments. RESULTS: Unadjusted, SNP RS4420638 within APOC1 was strongly associated with AD due entirely to linkage disequilibrium with APOE. In the multivariable adjusted analyses, 3 SNPs within the top 120 by P value in the logistic analysis and 1 in the Cox analysis of the Canadian data set provided additional evidence for association at P< .05 within the United Kingdom Medical Research Council data set: RS7019241 (GOLPH2), RS10868366 (GOLPH2), RS9886784 (chromosome 9), and RS10519262 (intergenic between ATP8B4 and SLC27A2). CONCLUSIONS: Our genomewide association analysis again identified the APOE linkage disequilibrium region as the strongest genetic risk factor for AD. This could be a consequence of the coevolution of more than 1 susceptibility allele, such as APOC1, in this region. We also provide new evidence for additional candidate genetic risk factors for AD that can be tested in further studies.
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rs541458 was directly genotyped in the extension sample, the TGEN study and the Li et al. study, with p<0.05 in each, and in meta-analysis it was one of the most significant SNPs (meta-p=8×10-10).
“This SNP is 8kb 5′ to the PICALM gene and was directly genotyped in the extension sample, the TGEN study and the Li et al. study, with p<0.05 in each.Following meta-analysis, this is one of our most significant SNPs (meta-p= 8×10 -10 )”
From Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer's disease (2009) · cites this paper as [8]
Prior genome-wide association studies of AD all identified strong evidence for association to APOE but less convincing evidence implicating other genes.
“All have identified strong evidence for association to APOE, but less convincing evidence implicating other genes2 -9 .”
From Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer's disease (2009) · cites this paper as [8]
Seven of the earliest GWAS, each of which used less than 2,000 cases, identified only APOE as significantly associated with Alzheimer's disease.
“seven of the earliest GWAS, each of which used less than 2,000 cases, identified only APOE as significantly associated with AD [84–90].”
From Genetic architecture of Alzheimer's disease (2020) · cites this paper as [88]
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“In fact, seven of the earliest GWAS, each of which used less than 2000 cases, identified only APOE as significantly associated with AD (Feulner et al., 2010; Carrasquillo et al., 2009; Beecham et al., 2009; Bertram et al., 2008; Li et al., 2008; Abraham et al., 2008; Liu et al., 2007).”
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- Authors
- Li, H., Wetten, S., Li, L., St. Jean, P. L., Upmanyu, R., Surh, L., Hosford, D., Barnes, M. R., Briley, J. D., Borrie, M., Coletta, N., Delisle, R., Dhalla, D., Ehm, M. G., Feldman, H. H., Fornazzari, L., Gauthier, S., Goodgame, N., Guzman, D., Hammond, S., Hollingworth, P., Hsiung, G.-Y., Johnson, J., Kelly, D. D., Keren, R., Kertesz, A., King, K. S., Lovestone, S., Loy-English, I., Matthews, P. M., Owen, M. J., Plumpton, M., Pryse-Phillips, W., Prinjha, R. K., Richardson, J. C., Saunders, A., Slater, A. J., St. George-Hyslop, P. H., Stinnett, S. W., Swartz, J. E., Taylor, R. L., Wherrett, J., Williams, J., Yarnall, D. P., Gibson, R. A., Irizarry, M. C., Middleton, L. T., & Roses, A. D.
- ORCID
- Li, Hao
- Wetten, Sally
- Barnes, Michael R.
- Ehm, Margaret G.
- Feldman, Howard H.
- Gauthier, Serge
- Goodgame, Neil
- Hsiung, Ging-Yuek
- Keren, Ron
- Kertesz, Andrew
- King, Karen S.
- Lovestone, Simon
- Matthews, Paul M.
- Owen, Michael J.
- Prinjha, Rab K.
- Richardson, Jill C.
- Saunders, Ann
- Taylor, Rachel L.
- Williams, Julie
- Gibson, Rachel A.
- Irizarry, Michael C.
- Middleton, Lefkos T.
- Venue
- Archives of Neurology
- Publisher
- American Medical Association (AMA)
- Published
- 2008-01-01
- Volume
- 65
- Issue
- 1
- Pages
- 45-53
- ISSN
- 0003-9942 (ISSN-L)
- OpenAlex
- W2145492845
- Cited by
- 499
- References
- 36
- Citations by year
- 2026: 1 · 2025: 10 · 2024: 7 · 2023: 9 · 2022: 12 · 2021: 14 · 2020: 20 · 2019: 13 · 2018: 19 · 2017: 25 · 2016: 26 · 2015: 19 · 2014: 33 · 2013: 31 · 2012: 45
- FWCI
- 36.00
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Archives of Neurology (publishedVersion)
- PubMed (publishedVersion)
- Research Portal (King's College London) (submittedVersion)
- Funders
- Wellcome Trust (081864)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- Alzheimer's disease, single nucleotide polymorphisms, genetic susceptibility, age of onset, apolipoprotein E, APOC1, linkage disequilibrium, SLC27A2, late-onset Alzheimer's disease, genetic risk factors, candidate genes, memory clinic patients, replication study
- MeSH terms
- Age Factors, Aged, Alzheimer Disease, Apolipoproteins E, Canada, Education, Female, France, Genotype, United Kingdom, Humans, Male, Registries, Sex Factors, Genome, Human, Confidence Intervals, Logistic Models, Proportional Hazards Models, Odds Ratio, Case-Control Studies, Oligonucleotide Array Sequence Analysis, Polymorphism, Single Nucleotide
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