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Genome-wide association study of the rate of cognitive decline in Alzheimer’s disease
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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].”
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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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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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