Evidence map›Paper›PMID 38724736›Full record

ArticleNature aging2024

Aging clocks based on accumulating stochastic variation.

David H Meyer, Björn Schumacher

Abstract read
In one paragraph

Article in Nature aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing 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

87 citing papers in PubMed.

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  9. Reversing aging-like 3D genome disorganization in abioRxiv : the preprint server for biology · 2026
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27 more citing papers are in PubMed but not listed here.

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

2 authors.

David H MeyerInstitute for Genome Stability in Aging and Disease, University Hospital and University of Cologne, Cologne, Germany. david.meyer@uni-koeln.de.ORCID http://orcid.org/0000-0002-5667-4720
Björn SchumacherInstitute for Genome Stability in Aging and Disease, University Hospital and University of Cologne, Cologne, Germany. bjoern.schumacher@uni-koeln.de.ORCID http://orcid.org/0000-0001-6097-5238

Funding

EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020) H2020-MSCA-ITN-2018 (Healthage and ADDRESS ITNs)John Templeton Foundation (JTF) 61734
6 · The paper itself

Abstract

Aging clocks have provided one of the most important recent breakthroughs in the biology of aging, and may provide indicators for the effectiveness of interventions in the aging process and preventive treatments for age-related diseases. The reproducibility of accurate aging clocks has reinvigorated the debate on whether a programmed process underlies aging. Here we show that accumulating stochastic variation in purely simulated data is sufficient to build aging clocks, and that first-generation and second-generation aging clocks are compatible with the accumulation of stochastic variation in DNA methylation or transcriptomic data. We find that accumulating stochastic variation is sufficient to predict chronological and biological age, indicated by significant prediction differences in smoking, calorie restriction, heterochronic parabiosis and partial reprogramming. Although our simulations may not explicitly rule out a programmed aging process, our results suggest that stochastically accumulating changes in any set of data that have a ground state at age zero are sufficient for generating aging clocks.

Indexed as

AgingDNA MethylationStochastic ProcessesAnimalsBiological ClocksCaloric RestrictionComputer SimulationHumansMaleModels, BiologicalParabiosisSmokingTranscriptome

Identifiers

PMID38724736
PMCPMC11186771

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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.