ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2026
Accelerated epigenetic aging as a modifier of homocysteine-associated cognitive decline: Findings from NHANES.
Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Apolipoprotein B100 and white matter hyperintensity as distinct mediators of thrombolytic response in acute stroke: preliminary findings.Journal of thrombosis and thrombolysis · 2026Article
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Authors and funding
12 authors.
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Abstract
introductionHyperhomocysteinemia represents a modifiable risk factor for cognitive decline and dementia, yet the role of epigenetic aging mechanisms in mediating this association remain poorly characterized, limiting development of targeted interventions.
methodsWe analyzed 1343 National Health and Nutrition Examination Survey participants aged ≥ 60 years using weighted regression, cubic splines, and mediation analyses. An independent cohort of 2073 participants validated findings.
resultsElevated homocysteine concentrations were significantly associated with reduced cognitive processing speed. GrimAge2 epigenetic age acceleration significantly mediated this association, accounting for 33.3% of the total effect. β2-microglobulin emerged as the strongest mediating component, explaining 38.8% of the homocysteine-cognition relationship. Folate demonstrated cognitive protection through homocysteine reduction (18.7% of total effect) without modulating downstream pathological cascades.
conclusionEpigenetic aging-associated neuroinflammation serves as a key mechanistic link between hyperhomocysteinemia and cognitive decline. The neuroprotective effects of folate are mediated specifically through homocysteine reduction, providing novel mechanistic insights for precision prevention strategies in cognitive aging.
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