Despite high abundance of OPCs in the aged brain, OPC proliferation and differentiation is slow and inefficient. We recently found that exposure to young CSF or to the growth factor Fgf17 boosted OPC proliferation and myelination capacity with aging. However, the underlying cellular mechanisms of oligodendrocyte dysfunction with aging are mostly unknown. Combining labeling of proliferating cells with transcriptomics and proteomic profiling we aim to elucidate underlying mechanisms of failed oligodendrogenesis with aging and facilitate the discovery of novel strategies to rejuvenate oligodendrocytes to restore or maintain cognitive function with age.
