Fig. 2.

Mechanisms of white matter damage produced by cardiovascular risk factors and Aβ. Oxidative stress and inflammation induced by these factors are responsible for disruption of the functions of the neurovascular unit (see Fig. 1), which, in turn, leads to local hypoxia–ischemia, axonal demyelination, and reduced repair potential of the white matter by altering oligodendrocyte progenitor cells. Data in autoimmune models of demyelination suggest that loss of myelin increases the energy consumption of the affected axons and aggravates local hypoxia. The resulting white matter damage contributes to both VCI and AD