Accelerated aging linked to cognitive decline in young cancer survivors

Researchers are shedding new light on how pediatric cancer survivorship affects aging and cognitive health decades after treatment. In a recent study, investigators examined both biologic and cognitive aging among young adult survivors of childhood cancer compared with their peers, finding evidence of accelerated aging and meaningful impacts on cognitive function and quality of life.

AnnaLynn M. Williams, PhD, assistant professor at the University of Rochester, explained that the research evaluated epigenetic aging—molecular changes that influence how genes function—as well as cognitive performance. Consistent with prior findings from the same cohort, survivors of pediatric cancer demonstrated accelerated epigenetic aging relative to individuals without a cancer history.

Importantly, the study went further by linking these biologic aging markers to cognitive outcomes. Across multiple measures of epigenetic aging, higher levels were associated with poorer cognitive performance, indicating a connection between molecular aging and neurocognitive decline.

Kevin Krull, PhD, member and chair at St. Jude Children’s Research Hospital, emphasized that these findings expand understanding of how cancer therapies affect long-term brain health. While cranial radiation and anti-folate therapies have long been recognized as neurotoxic, the results suggest that cancer treatment may also trigger broader molecular changes, such as DNA methylation, across multiple chemotherapy agents. Cognitive impairment, Krull noted, has wide-ranging implications for educational attainment, employment, social functioning, and overall quality of life, making these associations particularly significant for survivors.

The study also explored how treatment type influenced outcomes. Williams described dividing survivors into groups based on whether their therapies directly targeted the central nervous system. Regardless of treatment type, accelerated epigenetic aging was associated with worse cognitive outcomes, though patterns differed.

Survivors who received CNS-directed therapies more often showed memory impairments, while those without such treatments exhibited different cognitive profiles. Survivors of Hodgkin lymphoma appeared especially vulnerable, consistent with prior research showing heightened susceptibility to accelerated aging across biologic, physiologic, and cognitive domains.

Clinically, the findings suggest a need to broaden long-term monitoring for cognitive impairment beyond survivors exposed to traditionally neurotoxic treatments. Krull highlighted the importance of tracking patients who received anthracyclines, alkylating agents, and corticosteroids, in addition to cranial radiation and anti-folate therapies.

Beyond surveillance, the researchers emphasized intervention, noting that lifestyle factors such as physical activity, nutrition, sleep, and other health behaviors may help mitigate accelerated aging. Pharmacologic approaches may also play a role for some individuals.

Both experts underscored that accelerated aging in pediatric cancer survivors is an ongoing process that may manifest 20 to 30 years earlier than expected. Awareness of this trajectory is critical, as cognitive concerns in younger survivors should not be dismissed, even when individuals initially appear to be functioning well earlier in adulthood.

No relevant disclosures.

References

1. Researchers raise concerns about faster aging, possible early-onset dementia, for children and young adult cancer survivors. University of Rochester Medical Center. January 7, 2026. Accessed January 13, 2026. https://www.eurekalert.org/news-releases/1111871
2. Williams AM, Phillips NS, Dong Q, et al. Epigenetic age acceleration, telomere length, and neurocognitive function in long-term survivors of childhood cancer. Nat Commun. 2025. doi:10.1038/s41467-025-65664-5