A new study suggests that a specific “longevity gene” could help protect the brain from aging and Alzheimer’s disease.

Researchers at the Buck Institute for Research on Aging investigated how different variants of the APOE gene—known for its role in cholesterol transport—affect neurons in the brain.

The APOE4 variant is already associated with a higher risk of developing Alzheimer’s disease.

In contrast, APOE2 appears to reduce that risk and may even contribute to longer life spans.

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Using human brain cells derived from stem cells, the team found that neurons with APOE2 were better at repairing DNA damage and resisting “cellular senescence,” a process in which cells age and lose function.

Brain cells with APOE4, however, showed more damage and signs of decline. These findings were reinforced with follow-up studies in mice.

“We found that APOE2, a gene linked to exceptional longevity, helps human neurons better repair DNA damage and resist becoming senescent,” said senior author Lisa M. Ellerby, PhD, professor at the Buck Institute.

She explained that APOE is known for cholesterol transport, but this newly identified mechanism may explain why APOE2 carriers tend to live longer and face lower Alzheimer’s risk.

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Ellerby noted that her team was “very surprised” to discover how APOE2’s protective effects centered on DNA signaling and repair.

Adding the APOE2 protein to APOE4 neurons also reduced DNA damage following radiation stress, the study reported.

The results, published in Aging Cell, suggest that future therapies might aim to mimic APOE2’s benefits or strengthen brain DNA repair systems, particularly for people with the higher-risk APOE4 gene.

Christopher Weber, PhD, from the Alzheimer’s Association, called the research “an exciting and significant study” because it shifts attention toward how brain cells maintain their integrity as they age.

He said the findings open new directions for therapy development for APOE4 carriers.

The Alzheimer’s Association currently supports 13 projects in four countries studying APOE2’s role in Alzheimer’s protection, according to Weber.

“Supporting your brain’s DNA repair and slowing cellular senescence are good for you,” he added.

Caghan Kizil, PhD, of Columbia University, who was not involved in the research, said the study goes beyond the long-held link between APOE2 and longevity by showing how that protection might happen.

He said the work could help explain why certain brains stay more resilient with age and how natural protective mechanisms prolong brain health.

“Growing evidence suggests that APOE-related risk is not only about amyloid buildup but also how aging, inflammation, blood vessel health, and repair systems interact,” Kizil explained.

Both Weber and Kizil said future research could focus on what makes some brains more resilient and how those traits might be replicated in people with higher-risk genes.

“The long-term goal is to help vulnerable brains age more like resilient brains,” Weber said.

Ellerby emphasized that her team’s findings were based on lab experiments, not human trials. “Our study describes a biological mechanism and not a clinical treatment,” she said. “The precise molecular process still needs to be fully worked out.”

She cautioned against lifestyle changes or genetic testing based on this research alone.

However, she noted that maintaining DNA repair and slowing cellular decline supports overall brain health.

Healthy strategies mentioned by the researchers include exercising, getting good sleep, supporting cardiovascular health, and avoiding smoking and other “genotoxic” exposures.

“These are all super beneficial to your health, regardless of your APOE variant,” Ellerby said.