Alzheimer’s disease (AD) is the most common cause of dementia in the elderly. AD is pathologically characterized by β-amyloid (Aβ) plaques within the brain parenchyma and Aβ accumulation in blood vessels (cerebral amyloid angiopathy; CAA), as well as by the formation of neurofibrillary tangles and neurodegeneration (Duyckaerts et al., 2009). AD was not previously thought to be closely linked to cerebrovascular disease (CVD), but accumulating lines of evidence have shown a strong relationship between AD and vascular dementia (VaD) (Fotuhi et al., 2009; Kalaria and Ihara, 2013). AD and CVD share common risk factors (Viswanathan et al., 2009; Kalaria et al., 2012), and treatment of vascular risk factors is associated with slower decline in cognitive impairments of AD patients (Deschaintre et al., 2009). The Nun study revealed that CVD plays an important role in determining the presence and severity of the clinical symptoms of AD (Snowdon et al., 1997). Aβ accumulation and other AD changes are also recognized in elderly patients without apparent dementia (Funato et al., 1998; Schneider et al., 2007), which implies a strong relationship between AD neuropathology
