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Researchers identified 17 plasma proteins associated with all-cause mortality in older adults and found that several also tracked with biological-age measures. The findings were replicated in a second cohort, but they do not show that the proteins cause aging or provide a clinical test for predicting an individual’s lifespan.
A study published in Geromedicine has identified 17 plasma proteins associated with all-cause mortality in older adults, with several also linked to blood-test findings related to health risks and biological-age measures across multiple organ systems. The researchers tested their findings in a second group of participants, but the results show statistical associations—not that the proteins cause aging or can predict an individual’s lifespan.
In the 2026 paper in Geromedicine, Garvey and colleagues analyzed levels of 4,265 proteins in blood samples from 1,025 older adults in the LonGenity study. Participants were followed for an average of 8.05 years. The researchers used statistical models to assess associations between protein levels and death from any cause, then examined links with chronic disease burden and protein-based measures of biological age.
According to the study, higher levels of ERBB1, also called epidermal growth factor receptor, and ANTXR2 were associated with lower mortality risk and younger biological-age measures across multiple organ systems. Higher levels of MIC-1/GDF15, HE4 and IGFBP-2 were associated with higher mortality risk and older biological age across multiple systems.
The paper also reported more specific associations: elevated MIC-1/GDF15 was linked to older organismal biological age, while ERBB1 was associated with younger liver biological age. The authors evaluated their findings in 1,124 participants from the Baltimore Longitudinal Study of Aging and reported replication of key associations.
Protein Signals Across Organ Systems
The findings add evidence that blood proteins associated with mortality may also reflect differences in how the body and individual organs age. That overlap could help researchers investigate biological processes connecting systemic stress, chronic disease and physiological function, rather than relying on chronological age alone.
The proteins are candidates for further research, not established tools for personal health decisions. The study does not show that changing protein levels would reduce mortality, and it does not present a validated clinical blood test to estimate an individual’s lifespan or disease outcome.
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Two Cohorts, One Protein Analysis
Chronological age counts the years a person has lived, while biological-age measures aim to capture aspects of the body’s condition and aging. People of the same chronological age can differ in health, disease burden and resilience, a variation that the study sought to examine through blood-protein patterns.
As described in the paper by Garvey and colleagues, the analysis drew on the LonGenity cohort and then assessed key findings in the Baltimore Longitudinal Study of Aging. The report describes a longitudinal analysis of mortality associations and a separate evaluation of relationships with disease burden and proteome-derived biological-age measures. The open-access paper was published in Geromedicine in 2026.
Association Is Not Causation
The study does not establish whether the identified proteins contribute to aging or mortality, or whether their levels reflect other underlying processes. Although the authors reported that key associations were replicated in a second cohort, the results do not establish how well these proteins would predict outcomes for individuals outside the study groups.
The paper does not describe a clinical test, treatment strategy or threshold for interpreting any of the protein levels. Further mechanistic and clinical research is needed to determine whether these signals have practical value for assessing healthy aging or longevity.
Further Testing of Candidate Biomarkers
The researchers identify the proteins as candidates for future study of healthy aging and longevity. Further work would need to examine the biological mechanisms behind the associations and test whether the findings hold in additional populations and clinical settings.
Until that evidence is available, the results should be understood as research findings about groups of older adults—not as a way to forecast an individual’s lifespan. The study provides no announced timetable for follow-up research or clinical testing.
Key Questions
What did the study find?
In their paper in Geromedicine, Garvey and colleagues reported 17 plasma proteins associated with all-cause mortality among older adults. Several were also linked to biological-age measures across multiple organ systems.
Which proteins were linked to lower mortality risk?
The study reported that higher levels of ERBB1 and ANTXR2 were associated with lower mortality risk and younger biological-age measures across multiple organ systems. The findings do not show that these proteins cause those outcomes.
Which proteins were linked to higher mortality risk?
According to the study, higher levels of MIC-1/GDF15, HE4 and IGFBP-2 were associated with higher mortality risk and older biological age across multiple organ systems.
Can these findings predict how long someone will live?
No. The study did not establish a clinical test for predicting an individual’s lifespan or disease outcome. It reports statistical associations in two research cohorts.
Were the findings checked in another group?
Yes. The researchers evaluated their findings in 1,124 participants from the Baltimore Longitudinal Study of Aging and reported that key associations were independently replicated.
Source: news-medical.net
