The DOI matches its Crossref record; 33 of the 34 references it cites were found in a registry or an index.
Genome-wide association study of the rate of cognitive decline in Alzheimer’s disease
Open accessAbstract
Background: Substantial interindividual variability exists in the disease trajectories of Alzheimer's disease (AD) patients. Some decline rapidly whereas others decline slowly, and there are no known explanations for this variability. We describe the first genome‐wide association study to examine rate of cognitive decline in a sample of AD patients with longitudinal measures of cognition. Methods: The discovery sample was 303 AD cases recruited in the Alzheimer's Disease Neuroimaging Initiative and the replication sample was 323 AD cases from the Religious Orders Study and Rush Memory and Aging Project. In the discovery sample, Alzheimer's Disease Assessment Scale–cognitive subscale responses were tested for association with genome‐wide single‐nucleotide polymorphism (SNP) data using linear regression. We tested the 65 most significant SNPs from the discovery sample for association in the replication sample. Results: We identified SNPs in the spondin 1 gene ( SPON1 ), the minor alleles of which were significantly associated with a slower rate of decline (rs11023139, P = 7.0 × 10 −11 ) in the discovery sample. A SPON1 SNP 5.5 kb upstream was associated with decline in the replication sample (rs11606345, P = .002). Conclusion: SPON1 has not been previously associated with AD risk, but is plausibly related because the gene product binds to the amyloid precursor protein and inhibits its cleavage by β‐secretase. These data suggest that SPON1 may be associated with the differential rate of cognitive decline in AD.
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“Analysis of loci that reach GWAS and nominal significance and SNPs in LD with them at D’ ≥ 0.8 reveals predominant associations with traits such as cognitive decline [12, 68, 69], educational attainment [70–73], mean bone density [57, 74], intelligence and performance intelligence quotient [75, 76] and soluble TREM-2 levels [77].”
From Genetic drivers of progression in Alzheimer’s disease are distinct from disease risk (2026) · cites this paper as [12]
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“Lastly, genome wide analyses have often been confounded by the absence of disease confirmatory biomarkers such as amyloid, which is critical given the high rate of clinical misdiagnosis[12–14].”
From Genetic drivers of progression in Alzheimer’s disease are distinct from disease risk (2026) · cites this paper as [12]
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“In addition, we found the APOE and APP subnetwork within the vesicle mediated transport pathway which are among the most significant genetic risk factors for AD (Figure 5F).46,47,48”
From SCING: Inference of robust, interpretable gene regulatory networks from single cell and spatial transcriptomics (2023) · cites this paper as [48]
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McKhann, G., Drachman, D., Folstein, M., Katzman, R., Price, D., & Stadlan, E. M. (1984) · Neurology · doi:10.1212/wnl.34.7.939 · Cited by 27,915
Kok, J. S., Berg, I. J., & Scherder, E. J. A. (2013) · Dementia and Geriatric Cognitive Disorders Extra · doi:10.1159/000353441 · Cited by 20,589
Principal components analysis corrects for stratification in genome-wide association studies
Price, A. L., Patterson, N. J., Plenge, R. M., Weinblatt, M. E., Shadick, N. A., & Reich, D. (2006) · Nature Genetics · doi:10.1038/ng1847 · Cited by 10,248
A map of human genome variation from population-scale sequencing.
The 1000 Genomes Project Consortium (2010) · Nature · doi:10.1038/nature09534 · Cited by 7,877
METAL: fast and efficient meta-analysis of genomewide association scans
Willer, C. J., Li, Y., & Abecasis, G. R. (2010) · Bioinformatics · doi:10.1093/bioinformatics/btq340 · Cited by 5,205
A second generation human haplotype map of over 3.1 million SNPs
The International HapMap Consortium (2007) · Nature · doi:10.1038/nature06258 · Cited by 4,438
A new rating scale for Alzheimer's disease
(1984) · American Journal of Psychiatry · doi:10.1176/ajp.141.11.1356 · Cited by 4,175
Harold, D., Abraham, R., Hollingworth, P., Sims, R., Gerrish, A., Hamshere, M. L., Pahwa, J. S., Moskvina, V., Dowzell, K., Williams, A., et al. (2009) · Nature Genetics · doi:10.1038/ng.440 · Cited by 3,326
A genome-wide association study of type 2 diabetes in Finns detects multiple susceptibility variants
Scott, L. J., Mohlke, K. L., Bonnycastle, L. L., Willer, C. J., Li, Y., Duren, W. L., Erdos, M. R., Stringham, H. M., Chines, P. S., Jackson, A. U., et al. (2007) · Science · doi:10.1126/science.1142382 · Cited by 2,753
Genome-wide association study identifies variants at CLU and CR1 associated with Alzheimer's disease
the European Alzheimer's Disease Initiative Investigators, Lambert, J.-C., Heath, S., Even, G., Campion, D., Sleegers, K., Hiltunen, M., Combarros, O., Zelenika, D., Bullido, M. J., et al. (2009) · Nature Genetics · doi:10.1038/ng.439 · Cited by 2,234
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The ENIGMA Consortium: large-scale collaborative analyses of neuroimaging and genetic data
the Alzheimer’s Disease Neuroimaging Initiative, E. C., Thompson, P. M., Stein, J. L., Medland, S. E., Hibar, D. P., Vasquez, A. A., Renteria, M. E., Toro, R., Jahanshad, N., Schumann, G., et al. (2014) · Brain Imaging and Behavior · doi:10.1007/s11682-013-9269-5 · Cited by 838
Self-citationAlzheimer’s Disease Genetics: From the Bench to the Clinic
Karch, C. M., Cruchaga, C., & Goate, A. M. (2014) · Neuron · doi:10.1016/j.neuron.2014.05.041 · Cited by 473
A statistical framework for cross-tissue transcriptome-wide association analysis
Hu, Y., Li, M., Lu, Q., Weng, H., Wang, J., Zekavat, S. M., Yu, Z., Li, B., Gu, J., Muchnik, S. K., et al. (2019) · Nature Genetics · doi:10.1038/s41588-019-0345-7 · Cited by 407
Self-citationDavies, G., Marioni, R. E., Liewald, D. C., Hill, W. D., Hagenaars, S. P., Harris, S. E., Ritchie, S. J., Luciano, M., Fawns-Ritchie, C., Lyall, D., et al. (2016) · Molecular Psychiatry · doi:10.1038/mp.2016.45 · Cited by 373
Weiner, M. W., Veitch, D. P., Aisen, P. S. S., Beckett, L. A., Cairns, N. J., Green, R. C., Harvey, D. J., Jack, C. R., Jagust, W. J., Morris, J. C., et al. (2017) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2016.11.007 · Cited by 325
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Metadata
- Authors
- Sherva, R., Tripodis, Y., Bennett, D. A., Chibnik, L. B., Crane, P. K., de Jager, P. L., Farrer, L. A., Saykin, A. J., Shulman, J. M., Naj, A., Green, R. C., & The GENAROAD Consortium, T. A. D. N. I.
- Affiliations
- Boston University (US)
- Department of Medicine (Biomedical Genetics) Boston University School of Medicine Boston MA USA
- Corresponding author
- Sherva, Richard
- ORCID
- Venue
- Alzheimer's & Dementia
- Publisher
- Wiley
- Published
- 2013-03-26
- Volume
- 10
- Issue
- 1
- Pages
- 45-52
- ISSN
- 1552-5260 (ISSN-L)
- 1552-5279
- PMC
- PMC3760995
- OpenAlex
- W2034937783
- Cited by
- 180
- References
- 34
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 23 · 2023: 18 · 2022: 15 · 2021: 15 · 2020: 18 · 2019: 12 · 2018: 14 · 2017: 15 · 2016: 11 · 2015: 11 · 2014: 14 · 2013: 3
- FWCI
- 9.21
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Alzheimer s & Dementia (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (U01 AG024904)
- National Institute on Aging
- National Institute of Biomedical Imaging and Bioengineering
- Dana Foundation (HG02213, AG027841)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- Alzheimer's disease
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Cognition Disorders, Female, Follow-Up Studies, Genotype, Humans, Male, Neuropsychological Tests, Phenotype, Extracellular Matrix Proteins, Polymorphism, Single Nucleotide, Apolipoprotein E4, Genome-Wide Association Study
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