Evidence map›Paper›PMID 28393276›Full record

ArticleJournal of neural transmission (Vienna, Austria : 1996)2017

Leukocyte telomere length is linked to vascular risk factors not to Alzheimer's disease in the VITA study.

Margareta Hinterberger, Peter Fischer, Klaus Huber, Walter Krugluger, Sonja Zehetmayer

Abstract read
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In one paragraph

Article in Journal of neural transmission (Vienna, Austria : 1996), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed.

  1. Trial
  2. Review
  3. Article
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  5. Article
  6. Article
  7. Review
  8. Review
  9. Observational
  10. Review
  11. Article
  12. Review
  13. Aging, Cellular Senescence, and Alzheimer's Disease.International journal of molecular sciences · 2022
    Review
  14. Article
  15. Article
  16. Cellular Senescence in Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2020
    Review
  17. Article
  18. Article
  19. Article
  20. Ageing, Cellular Senescence and Neurodegenerative Disease.International journal of molecular sciences · 2018
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Margareta HinterbergerMedical Research Society Vienna D.C., Danube Hospital (Former Ludwig Boltzmann Institute of Aging Research), Langobardenstraße 122, 1220, Vienna, Austria. margareta.hinterberger@utanet.at.ORCID 0000-0002-8422-0216
Peter FischerMedical Research Society Vienna D.C., Head of Department of Psychiatry, Danube Hospital, Langobardenstraße 122, 1220, Vienna, Austria.
Klaus HuberDepartment of Laboratory Diagnostics, Danube Hospital, Langobardenstraße 122, 1220, Vienna, Austria.
Walter KruglugerDepartment of Laboratory Diagnostics, Danube Hospital, Langobardenstraße 122, 1220, Vienna, Austria.
Sonja ZehetmayerSection for Medical Statistics, Medical University of Vienna, Spitalgasse 23, 1090, Vienna, Austria.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Association of telomere shortening with overall dementia or Alzheimer's disease is described controversially and the pathophysiologic relevance is unclear. Whether patients, suffering from pure probable Alzheimer's disease or pure vascular dementia, have shorter leukocyte telomeres than cognitively healthy controls was determined. Leukocyte telomere lengths (LTLs) of 597 participants of the VITA study (longitudinal community-based age-cohort [mean 75.7 (±0.45) years] study: 243 male; 578 non-demented at baseline) were compared with different aspects of cognition, risk factors of dementia and survival. LTLs of 264 persons cognitively healthy at baseline (mild cognitive impaired excluded) and all follow-ups (mean = 5643 bp, SD = 736) did not show any difference to LTLs of 43 incident pure possible (mean = 5548 bp; SD = 666) or 34 incident pure probable Alzheimer's diseases (mean = 5712 bp; SD = 695; post hoc Dunnett test: MD = -95; SE = 119; p = 0.67 and MD =+68.3; SE = 132; p = 0.84, res.). 264 stably cognitively healthy showed a trend to longer telomeres than 6 incident vascular dementias (mean = 5643 bp, SD = 736 vs mean = 5101 bp, SD = 510; t test: T = 1.8; df = 268; p = 0.07). Males (n = 243; mean = 5470 bp; SD = 684) had significantly shorter telomeres than females (n = 354; mean = 5686 bp; SD = 714; t test: T = -3.7; df = 595; p = 0.0001) and died significantly earlier (113.7 vs 130.1 months: Log Rank Chi square = 12.2; p = 0.0001). Shorter telomeres were associated with prevalence of more than one vascular risk factor (n = 587; mean = 5728; SD = 723 vs mean = 5533; SD = 691; t test: T = 3.1; df = 576; p = 0.002) and, as a trend, with poorer survival (Cox Regression: Wald = 4.9; p = 0.026; OR = 0.98; 95% CI 0.96-0.99). In 75.7 years old persons, no association of LTL with incident pure Alzheimer's disease was found. Significantly shorter telomeres were associated with sum of vascular risk factors, males and early mortality in males. Exclusion of mixed dementias may improve the search for risk factors more specific for Alzheimer's disease.

Indexed as

Telomere ShorteningAgedAged, 80 and overAlzheimer DiseaseCohort StudiesDementia, VascularFemaleHumansLeukocytesLongitudinal StudiesMaleRisk FactorsAlzheimer’s diseaseCardiovascular diseaseLeukocyte telomere lengthMixed dementiaVascular dementia

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Registered trials

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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.