Vasodilator dysfunction and oligodendrocyte dysmaturation in aging white matter

Objective Microvascular brain injury (mVBI) is a common pathologic correlate of vascular contributions to cognitive impairment and dementia (VCID) that leads to white matter injury (WMI). VCID appears to arise from chronic recurrent white matter ischemia that triggers oxidative stress and an increase in total oligodendrocyte lineage cells. We hypothesized that mVBI involves vasodilator dysfunction of white matter penetrating arterioles and aberrant oligodendrocyte progenitor cell (OPC) responses to WMI.