ArticleMedicine2026
Association of telomere length with cognitive function and dementia: A cross-sectional NHANES analysis and 2-sample Mendelian randomization study.
Article in Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
This study aimed to investigate the association between telomere length, cognitive function, and dementia, and to assess causality using Mendelian randomization (MR). This study included 1815 participants aged over 60 from the National Health and Nutrition Examination Survey (NHANES) conducted between 1999 and 2002. Cognitive function was assessed using the digit symbol substitution test score, and telomere length was quantified as the mean leukocyte telomere length (telomere/single-copy gene) measured by quantitative polymerase chain reaction. Weighted multivariate linear regression was applied to examine the relationship between cognitive function and telomere length. Additionally, a 2-sample MR approach was employed to explore the genetic causal relationship between telomere length and dementia, and its subtypes, using summary-level genome-wide association studies data derived primarily from individuals of European ancestry. The primary analysis utilized inverse variance weighting, and a series of sensitivity analyses were conducted to ensure robustness of the results. In the cross-sectional observational analysis, longer telomere length was positively associated with higher digit symbol substitution test scores after full adjustment (T2 vs T1: β = 2.1, 95% confidence interval [CI]: 0.35-3.9, P = .022; T3 vs T1: β = 2.5, 95% CI: 0.69-4.3, P < .001). In the MR analysis, genetically predicted longer telomere length was causally associated with a reduced risk of all-cause dementia (odds ratio [OR] per 1-standard deviation increase: 0.90, 95% CI: 0.83-0.98, P = .017), Alzheimer's disease (OR: 0.87, 95% CI: 0.76-0.99, P = .036), and vascular dementia (OR: 0.80, 95% CI: 0.65-0.97, P = .026). However, no causal association was found with frontotemporal dementia or Parkinson's disease. Observational and genetic evidence jointly suggest that longer telomere length is associated with better cognitive function and may play a protective causal role against major forms of dementia.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.