Fig. 2

AD pathology and alterations in OPC-related events under pathological circumstances of AD. Under AD pathological conditions, alterations in mitochondrial structure and function result in an overproduction of reactive oxygen species (ROS), leading to oxidative damage of subcellular structures and fragmentation of mitochondria. The oxidative damage and mitochondrial fragmentation further induce inflammatory responses, involving changes in microglial and astrocyte phenotypes. Pro-inflammatory DAM type microglia and DAA type astrocytes release pro-inflammatory cytokines, exacerbating mitochondrial dysfunction and oxidative stress, culminating in a vicious cycle termed “mitochondrial dysfunction-oxidative stress-inflammation response.” Consequently, these changes exacerbate the AD pathology. Within unfavorable cerebral microenvironment, OPC myelination-related events are adversely affected to varying degrees