This drainage route closely corresponds with the distribution of Aβ in the basement membranes of capillary and artery walls in CAA (Weller et al., 1998), which implies that the congestion of drainage pathway is associated with the pathogenesis of CAA. The fact that CAA was accelerated in the brains of immunized AD patients and that the CSF Aβ concentration was decreased both in AD and CAA patients may result from an impaired perivascular drainage pathway (Nicoll et al., 2004; Patton et al., 2006; Verbeek et al., 2009). Consistent with this, perivascular drainage of solutes is impaired in the aging mouse brain and in the presence of CAA (Hawkes et al., 2011). The fact that cerebral Aβ clearance was delayed after photothrombosis within individual vessels or middle cerebral artery occlusion (Garcia-Alloza et al., 2011), and after bilateral common carotid artery stenosis (Okamoto et al., 2012), further supports the notion that brain ischemia and impaired arterial pulsation could be an exacerbation factor of CAA. Consistent with the experimental data is the clinical finding that arterial stiffness, indicated by pulse wave velocity, has
