Abstract
There is substantial controversy regarding the causative role of amyloid β (Aβ) deposition in Alzheimer's disease (AD). The cerebrovasculature plays an important role in the elimination of Aβ from the brain and hypertension is a well-known risk factor for AD. In spontaneously hypertensive stroke-prone rats (SHRSP), an animal model of chronic arterial hypertension, cerebral small vessel disease (CSVD) leads to age-dependent parenchymal Aβ accumulation similar to that observed in AD. These data approve the neuropathological link between CSVD and AD, confirm the challenge that parenchymal Aβ deposition is a specific marker for AD and disclose the meaning of SHRSP as valid experimental model to investigate the association between hypertension, CSVD, and Aβ plaques.