ArticleGeroScience2025
Alzheimer's Disease polygenic risk, the plasma proteome, and dementia incidence among UK older adults.
Article in GeroScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Article
- Polygenic risk for depression is associated with post-stroke depression and stroke.IBRO neuroscience reports · 2026Article
- Plasma proteomics ofmedRxiv : the preprint server for health sciences · 2026Article
- Integrative machine learning approach to risk prediction for dementia and Alzheimer's disease.GeroScience · 2026Article
- Adhesion molecules provide an endothelial protein signature in preclinical and clinical Alzheimer's disease and predict clinical progression.Communications medicine · 2026Article
- Metabolic signatures, vitamin D, and red cell distribution width in dementia risk: UK Biobank insights.GeroScience · 2026Article
- Alzheimer's disease polygenic risk's association with all-cause dementia through the plasma metabolome in the UK Biobank study.GeroScience · 2025Article
- Integrating genetic and immune profiles for personalized immunotherapy in Alzheimer's disease.Frontiers in medicine · 2025Review
- NFκB1: a common biomarker linking Alzheimer's and Parkinson's disease pathology.Frontiers in neuroscience · 2025Article
- The proteomic and metabolomic signature of inherited chromosomally integrated HHV-6 and its role in all-cause dementia and mortality risk: The UK Biobank study.Alzheimer's & dementia (New York, N. Y.)Article
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11 authors.
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Abstract
Alzheimer's Disease (AD) is a complex polygenic neurodegenerative disorder. Its genetic risk's relationship with all-cause dementia may be influenced by the plasma proteome. Up to 40,139 UK Biobank participants aged ≥ 50y at baseline assessment (2006-2010) were followed-up for ≤ 15 y for dementia incidence. Plasma proteomics were performed on a sub-sample of UK Biobank participants (k = 1,463 plasma proteins). AD polygenic risk scores (PRS) were used as the primary exposure and Cox proportional hazards models were conducted to examine the AD PRS-dementia relationship. A four-way decomposition model then partitioned the total effect (TE) of AD PRS on dementia into an effect due to mediation only, an effect due to interaction only, neither or both. The study found that AD PRS tertiles significantly increased the risk for all-cause dementia, particularly among women. The study specifically found that AD PRS was associated with a 79% higher risk for all-cause dementia for each unit increase (HR = 1.79, 95% CI: 1.70-1.87, P < 0.001). Eighty-six plasma proteins were significantly predicted by AD PRS, including a positive association with PLA2G7, BRK1, the glial acidic fibrillary protein (GFAP), neurofilament light chain (NfL), and negative with TREM2. Both GFAP and NfL significantly interacted synergistically with AD PRS to increase all-dementia risk (> 10% of TE is pure interaction), while GFAP was also an important consistent mediator in the AD PRS-dementia relationship. In summary, we detected significant interactions of NfL and GFAP with AD PRS, in relation to dementia incidence, suggesting potential for personalized dementia prevention and management.
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