T cell-mediated microglial activation triggers myelin pathology in a mouse model of amyloidosis.
Shreeya KediaHao JiRuoqing FengPeter AndrovicLena SpiethLu LiuJonas FranzHanna ZdiarstekKatrin Perez AndersonCem KabogluQian LiuNicola MattuginiFatma CherifDanilo PrtvarLudovico Cantuti-CastelvetriArthur LieszMartina FettingChristine StadelmannSabina TahirovicOzgun GokceMikael SimonsPublished in: Nature neuroscience (2024)
Age-related myelin damage induces inflammatory responses, yet its involvement in Alzheimer's disease remains uncertain, despite age being a major risk factor. Using a mouse model of Alzheimer's disease, we found that amyloidosis itself triggers age-related oligodendrocyte and myelin damage. Mechanistically, CD8 + T cells promote the progressive accumulation of abnormally interferon-activated microglia that display myelin-damaging activity. Thus, our data suggest that immune responses against myelinating oligodendrocytes may contribute to neurodegenerative diseases with amyloidosis.