A new study suggests the APOE2 gene may help neurons repair DNA damage and resist aging, offering clues to lower Alzheimer’s risk.
A gene variant long associated with longevity may help shield brain cells from Alzheimer’s-related vulnerability by improving DNA repair and slowing cellular aging, according to a new laboratory study.
Researchers at the Buck Institute for Research on Aging used human brain cells derived from stem cells to study APOE2, a variant of the APOE gene. APOE is best known for its role in moving and metabolizing fats and cholesterol, particularly in the brain. The APOE4 variant is linked to higher Alzheimer’s risk, while APOE2 has been associated with lower risk.
The study found that neurons with APOE2 were better able to repair DNA damage and resist cellular senescence, a state in which cells become aged and dysfunctional. Brain cells carrying APOE4 appeared more fragile and more likely to show signs of aging and dysfunction, the researchers reported. Follow-up studies in mice supported the findings.
“We found that APOE2, a gene linked to exceptional longevity (enriched in centenarians), helps human neurons better repair DNA damage and resist becoming senescent, or aged and dysfunctional,” senior author Lisa M. Ellerby, a professor at the Buck Institute, told Fox News Digital.
Ellerby said the finding may help explain why people with APOE2 tend to live longer and have lower Alzheimer’s risk. The researchers also reported that adding the APOE2 protein to APOE4 neurons reduced DNA damage after radiation exposure, suggesting a possible future direction for treatments designed to mimic APOE2’s protective effects or strengthen DNA repair in the brain.
The findings were published in the journal Aging Cell . Outside experts quoted by Fox News Digital described the work as significant because it points beyond APOE’s familiar cholesterol-related role and toward the way aging brain cells maintain their integrity over time.
Christopher Weber, senior director of global scientific initiatives at the Alzheimer’s Association, said the study “opens up some new directions for therapy development,” particularly for people who carry APOE4. The association has 13 active projects in four countries examining APOE2’s potential protective role, he said.
The researchers emphasized that the work remains early. Ellerby said the study describes a biological mechanism in human stem-cell-derived neurons and mice, not a clinical treatment. The precise molecular process by which APOE2 supports nuclear stability and repair still needs to be worked out.
She also cautioned that people should not change health behaviors or seek APOE genetic testing solely for longevity based on this study. General brain-health steps such as exercise, adequate sleep, cardiovascular health and avoiding exposures such as smoking remain beneficial regardless of APOE variant, she said.
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