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Researchers identified 17 plasma proteins associated with all-cause mortality among older adults, with several also linked to biological-age measures across organ systems. Key associations were replicated in a second cohort, but the study does not show that the proteins cause aging or can predict an individual’s lifespan.
A study published in Geromedicine identified 17 plasma proteins associated with all-cause mortality in older adults, and found that several were also linked to biological-age measures across multiple organ systems. The findings, based on two longitudinal cohorts, may help researchers investigate how health and aging differ among people of the same chronological age, but they do not establish that the proteins cause aging or predict an individual’s lifespan.
The researchers measured 4,265 proteins in blood samples from 1,025 older adults enrolled in the LonGenity study. Participants were followed for an average of 8.05 years. Using statistical models, the team examined whether protein levels were associated with all-cause mortality, then assessed links with chronic disease burden and biological-age measures for the body and individual organs.
Higher levels of ERBB1 and ANTXR2 were associated with lower mortality risk and younger biological age across multiple organ systems. Higher levels of MIC-1/GDF15, HE4 and IGFBP-2, by contrast, were associated with higher mortality risk and older biological age across multiple systems. The report also describes more specific associations: elevated MIC-1/GDF15 was linked with older organismal biological age, while ERBB1 was linked with younger liver biological age.
The researchers tested key associations in an independent group of 1,124 participants from the Baltimore Longitudinal Study of Aging, reporting that they were replicated there. The study, by investigators from Albert Einstein College of Medicine, Stony Brook University, the National Institute on Aging and other institutions, is titled “Exploring mortality-linked proteins: Understanding their association with biological aging, disease phenotypes, signaling pathways, and their implications for longevity.”
Protein Signals Across Organ Systems
The results give geroscience researchers a set of candidate biomarkers to investigate as they study why people of similar chronological age can have different health, disease burdens and resilience. Because some mortality-associated proteins also tracked with age measures in several organs, the findings may help researchers examine whether biological aging has shared signals across the body or varies by organ.
That could guide future work on systemic stress, physiological homeostasis and chronic disease. But the associations are not evidence that changing a protein level would change a person’s health or lifespan. The report does not establish a clinical test, provide an individual risk estimate or show that the proteins can be used to select a treatment.
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Two Cohorts, One Protein Analysis
Chronological age records time lived; biological age is an effort to capture how rapidly the body, or a particular organ, may be aging. Researchers use biological-age measures to study differences in health that a person’s age in years alone may not reflect. This study examined whether proteins measured in blood were associated both with mortality and with these measures of aging.
The analysis used the LonGenity cohort to identify associations and the Baltimore Longitudinal Study of Aging to evaluate key findings independently. Replication in a second cohort lends support to the reported statistical relationships, while the study’s observational design means it cannot establish cause and effect. The work was published open access in Geromedicine in 2026.
“The findings may help researchers better understand the biological pathways that connect systemic stress, physiological homeostasis, chronic disease and aging.”
— The study authors, as described in the report
Cause, Prediction and Clinical Use
It remains unclear whether the proteins contribute to aging or mortality, reflect underlying health changes, or are associated with other factors. The study reports statistical relationships; it does not show that altering protein levels would reduce mortality or make organs biologically younger.
The findings also do not establish that a blood test based on these proteins can predict an individual’s lifespan or disease outcome. The report does not provide a clinical threshold, a validated personal-risk tool or evidence that the proteins improve decisions about care. Further research is needed to test how these signals work and whether they have practical value.
Testing the Signals Further
The next step is further mechanistic and clinical investigation of the proteins, including whether the reported links hold in other populations and how they relate to specific pathways, diseases and organ-level aging. Researchers would also need to establish whether protein measurements add useful information beyond other health measures before considering clinical applications.
No follow-up trial, clinical test or schedule for additional results is specified in the report. For now, the findings are best understood as research leads from two cohorts, not a basis for estimating an individual’s mortality risk.
Key Questions
What did the study find?
It identified 17 plasma proteins associated with all-cause mortality among older adults. Several were also associated with biological-age measures across multiple organ systems.
Which proteins were linked to lower mortality risk?
Higher levels of ERBB1 and ANTXR2 were associated with lower mortality risk and younger biological age across multiple organ systems. These are associations, not proof that the proteins protect against aging or death.
Which proteins were linked to higher mortality risk?
Higher levels of MIC-1/GDF15, HE4 and IGFBP-2 were associated with higher mortality risk and older biological age across multiple systems.
Can these proteins predict how long someone will live?
No individual lifespan test was established by this study. It reports associations in research cohorts and does not provide a validated clinical tool for predicting a person’s lifespan or disease outcome.
Were the findings checked in another group?
Yes. The researchers evaluated key associations in 1,124 participants from the Baltimore Longitudinal Study of Aging and reported independent replication. That supports the findings but does not establish causation or clinical usefulness.
Source: news-medical.net
