bioRxivNov 3, 2026, 15:04 GMT

Measures of aging in cell structures linked to disease risk

Among 61,931 people, four or more prematurely aged compartments were linked to up to 22-fold higher kidney disease risk and up to 8-fold higher mortality risk.

Paper by Albert Kejun Ying, Kyle KunHyung Roh, Kenneth L. Chen, +6Tony Wyss-Coray · Stanford University

Kidney cross-section with intact and fragmented tissue beside mitochondria with dense or broken folds, sparse or crowded lysosomes, and curved membrane stacks.

Our read

Biomarkers

Studied:: Preprint: study of 61,931 people across the human lifespan
What changed:: Kidney disease risk was up to 22-fold higher among people with four or more prematurely aged compartments
The catch:: Fluid proteins served as proxies for organelle aging rather than direct measurements inside cells
In the record:: The 989th paper on APOE with results in people; 3,736 on record in all.
Why it’s aging research:: It builds or tests a tool for aging research.

Editor of record: Boris Djordjevic · AgingResearch.News

Paper

Researchers analyzed protein measurements from 61,931 people in an observational study. The proteins came from blood plasma and cerebrospinal fluid, the fluid around the brain and spinal cord. They used proteins enriched in particular organelles—specialized structures within cells—to model the aging of 10 organelles across the human lifespan.

The estimated aging patterns differed among organelles. Estimates for lysosomes, which break down cellular waste, cells’ outer membranes and the Golgi apparatus, which processes and packages proteins, accelerated rapidly after age 60. More compartments with accelerated estimated aging were linked to higher disease risk. Different major diseases also had distinct patterns of estimated organelle aging.

Why it matters

Aging does not affect every cell structure alike. Measuring these differences may help researchers investigate why people vary in their susceptibility to disease.

Caveats

The observational analysis used protein-based estimates of organelle aging, so it cannot establish cause and effect. The preprint has not been peer-reviewed; its abstract does not specify the risk comparison groups or follow-up.