Aβ suppresses oligodendrocyte differentiation in vivo or vitro via inflammatory activation and cytoskeletal contraction [RNA-seq2]

Aβ disrupts oligodendrocyte lineage cells through a dual mechanism inflammatory activation and cytoskeletal compromise leading to maturation blockade and hypomyelination independent of axonal damage. These findings position oligodendrocyte dysfunction as a key component of AD white matter pathology and identify potential therapeutic targets.