Alzheimer's disease (AD) is a central nervous system degenerative disease with a stealthy onset and a progressive course characterized by memory loss, cognitive dysfunction, and abnormal psychological and behavioral symptoms. However, the pathogenesis of AD remains elusive. An increasing number of studies have shown that oligodendrocyte progenitor cells (OPCs) and oligodendroglial lineage cells (OLGs), especially OPCs and mature oligodendrocytes (OLGs), which are derived from OPCs, play important roles in the pathogenesis of AD. OLGs function mainly by myelinating axons, transmitting electrical signals, and regulating neural development. In addition to myelin, OPCs and OLGs can also participate in AD pathogenesis in other ways. This review summarizes the mechanisms by which OPCs and OLGs affect myelin formation, oxidative stress, neuroinflammation, the blood-brain barrier, synaptic function, and amyloid-beta protein and further elucidates the mechanisms by which oligodendrocyte lineage cells participate in AD pathogenesis and treatment, which is highly important for clarifying the pathogenesis of AD, clinical treatment, and prevention.
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