Longitudinal plasma proteomic aging clock in the KORA cohort
A plasma proteomic aging clock built on repeated measurements in the KORA cohort linked proteomic age acceleration to lifestyle and clinical risk factors and to all-cause mortality. [1]
Automatic summary · not editorially reviewed
The key findings
The final dataset comprised 9,105 plasma proteomics samples from 4,100 KORA cohort individuals aged 25–88 years, measured at up to three time points. [1]
Higher proteomic age acceleration was associated with increased all-cause mortality, and mediation analysis suggested risk factors were linked to mortality indirectly through age acceleration. [1]
Mendelian randomization identified proteins with evidence consistent with a causal role in aging-related traits. [1]
The source at a glance
- Study type / format
- Longitudinal cohort study using plasma proteomics (abstract).
- Population / context
- 4,100 participants of the population-based KORA cohort aged 25–88 years, with 9,105 plasma samples.
- Summary based on
- Study abstract
- Publication status
- Preprint · peer-review status not confirmed
- Original publication
- October 6, 2026
Repeated plasma proteomics in 4,100 KORA participants
Most proteomic aging clocks rely on cross-sectional data. This study instead used longitudinal measurements of liquid chromatography–mass spectrometry plasma proteomics at up to three time points in the population-based KORA cohort. The final dataset comprised 9,105 samples from 4,100 individuals aged 25–88 years. The model predicts chronological age and yields a measure of proteomic age acceleration.
Supporting source [1]
Risk factors, mortality and suggested mediation
Proteomic age acceleration was associated with lifestyle and clinical risk factors. Risk factor–stratified analyses showed shared proteomic signatures among cardiometabolic exposures and distinct signatures for smoking and physical activity. Within individuals, dyslipidemia and impaired kidney function tracked transitions to increases in age acceleration. Higher age acceleration was associated with increased all-cause mortality, and mediation analysis suggested risk factors were linked to mortality indirectly through age acceleration.
Supporting source [1]
Proteins, pathways and Mendelian randomization signals
Affected proteins and pathways highlighted extracellular matrix remodeling, complement and coagulation pathways, and liver-derived plasma proteins as key contributors to aging. Mendelian randomization identified proteins with evidence consistent with a causal role in aging-related traits. The authors conclude the findings are consistent with biological aging being dynamically responsive to changes in modifiable risk factors; these are associations, not proof that changing risk factors causes slower aging.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. The abstract reports associations and mediation results, not that modifying risk factors slows aging. Mendelian randomization findings are described only as evidence consistent with a causal role.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Lermer R, Qian X, Pusch S, Schaefer T, Adam J, Li L, von Scheidt M, Linkohr B, Peters A, Mann M, Schunkert H, Heinig M. · europepmc.org · October 6, 2026