Abstract
Roles of oligodendrocyte (OL) lineage cells in the pathogenesis of Alzheimer's disease (AD) have been elusive. We established a method for purifying and culturing adult OL progenitor cells (aOPCs) from the rat hippocampus and report novel aOPCs expressing plexin-B3 as amyloid b (Ab) secreting cells. Plexin-B3+ aOPCs was persistently contaminated in the proliferating aOPC cultures with fibroblast growth factor 2 (FGF2). FGF2 withdrawal increased plexin-B3+ but decreased NG2+ aOPCs, with unique senile plaque-like morphological changes and increased Ab1–42 secretion. In vivo, plexin-B3+ aOPCs distributed throughout the adult rat brain but much less densely than do NG2+ aOPCs. Spreading depolarization, a common mechanism of cortical injuries, induced unique delayed plexin-B3+ oligodendrogliosis in the ipsilateral but not contralateral remote cortex. In AD brains, senile plaques were mostly immunostained with plexin-B3 antibodies. These findings suggest that plexin-B3+ aOPCs play essential roles in the pathogenesis of AD as Ab secreting cells.
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