Nature medicine · 2026
Oligodendrocyte dysfunction in human age-related cognitive decline.
СтатьяНазвание и аннотация: Перевод в очереди
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Craig Georgina A, Merour Emeric, Seeker Luise A, Haughian Annette J, Arbabi Keon, Rose Jamie, Hoffmann Alana, Thapar Jessica, Corsinotti Andrea, Mitchell Stephen, Corley Janie, Shenkin Susan D, Smith Colin, Spires-Jones Tara L, Sun Lu O, Cox Simon R, Williams Anna, Tripathy Shreejoy J, Popko Brian, Miron Véronique E
Аннотация
Cognitive decline in aging impacts quality of life, for which therapeutic interventions are lacking. Why some individuals experience more severe cognitive decline with aging is unclear. Here we uncover a role for the brain's myelin-forming cells-oligodendrocytes-in explaining this variance. By investigating neuropathological and transcriptomic changes in human white matter associated with individual rates of cognitive decline in aging, we find that worse cognitive trajectories unexpectedly associate with smaller myelinated axon size, thicker myelin and more oligodendrocytes with downregulation of NRF2. Aged oligodendrocyte-specific NRF2-knockout mice showed attenuated cognitive improvement over time and mirrored the white matter pathology of human cognitive decline in aging. These findings place the oligodendrocyte as a contributor to cognitive decline and highlight the NRF2 pathway as a therapeutic target to preserve cognition in human aging.