'Despite these key cellular effects of Aβ, and its essential role in AD, the traditional assumption that neurons are the primary source of pathogenic Aβ in the brain has remained untested. In this study, we show that oligodendrocytes in human tissue contain all of the components required to produce Aβ, and that human oligodendrocytes produce soluble Aβ in vitro. We further show that selectively suppressing oligodendrocyte Aβ production in an AD mouse model is sufficient to rescue abnormal neuronal hyperactivity.'
https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.3002727