FIGURE 8.

Proposed model by which BCAS and amyloid may impact on glymphatic function and predispose to VCI. In the long-term response to BCAS, reduced arterial pulsatility may impede CSF influx along the periarterial space and contribute in part to amyloid accumulation within the parenchyma and vasculature. Independently amyloid (Aβ40) has a profound impact on arterial pulsatility and impedes CSF influx. Downstream these events may influence glial cell responses including reactive astrogliosis and inflammation that can contribute to VCI.