Epigenetic age acceleration, but not mean telomere length, linked to worse neurocognitive function
TUESDAY, Jan. 13, 2026 (HealthDay News) — For survivors of childhood cancer, epigenetic age acceleration (EAA) is associated with worse neurocognitive function, according to a study published online Nov. 27 in Nature Communications.
AnnaLynn M. Williams, Ph.D., from St. Jude Children”s Research Hospital in Memphis, Tennessee, and colleagues conducted a cross-sectional study involving 1,413 survivors of childhood cancer who completed a neuropsychological battery. The association between neurocognitive function and biologic aging was assessed using mean leukocyte telomere length residual (mLTL) and EAA from five different epigenetic clocks.
The researchers found an association for higher EAA, measured by PCGrimAge, or DunedinPACE with worse performance on multiple measures of attention, processing speed, and executive functions among survivors treated with central nervous system (CNS)-directed therapy. The results were similar for PCGrimAge among non-CNS-treated survivors, but DunedinPACE was specifically associated with attention variability. No association was seen for mLTL with neurocognition.
“Young cancer survivors have many more decades of life to live,” Williams said in a statement. “So if these accelerated aging changes are occurring early on and setting them on a different trajectory, the goal is to intervene to not only increase their lifespan but improve their quality of life.”
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