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Brain cells once thought to be purely protective may actually speed up cognitive decline as we age. Researchers found that oligodendrocytes — cells that maintain the insulating coating around nerve fibers — can become dysfunctional, producing abnormal myelin and damaging nerve fibers. The good news? Drugs already used for multiple sclerosis may offer a path to new treatments.
Scientists from the University of Edinburgh and the UK Dementia Research Institute have flipped the script on a long-held assumption: brain cells called oligodendrocytes, traditionally seen as purely beneficial, may actually contribute to age-related cognitive decline. Published in Nature Medicine, the study found that as these cells age, they can become dysfunctional — producing abnormal myelin (the protective coating around nerve fibers) and ultimately damaging the very fibers they're meant to support.
The research drew on decades of cognitive tracking data from the Lothian Birth Cohort 1936, alongside post-mortem brain tissue analysis. People with greater cognitive decline had fewer large nerve fibers and more abnormal myelin buildup. The culprit? Lower levels of a protein called NRF2 inside oligodendrocytes — a key regulator of cellular defense. Mouse experiments confirmed that reducing NRF2 in these cells replicated the same brain abnormalities and worsened cognitive performance.
Key Takeaways:
Why it matters: With no current treatments for age-related cognitive decline and a rapidly aging global population, identifying a druggable biological pathway is a significant step forward. The fact that NRF2-targeting medications already exist makes this discovery especially actionable for future clinical development.