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We aimed to test the hypothesis that in spontaneously hypertensive stroke‐prone rats ( SHRSP ), non‐amyloid cerebral small vessel disease/hypertensive arteriopathy ( HA ) results in vessel wall injury that may promote cerebral amyloid angiopathy ( CAA ). Our study comprised 21 male  SHRSP  (age 17–44 weeks) and 10 age‐ and sex‐matched Wistar control rats, that underwent two‐photon (2 PM ) imaging of the arterioles in the parietal cortex using Methoxy‐X04, Dextran and cerebral blood flow ( CBF ) measurements. Our data suggest that  HA  in  SHRSP  progresses in a temporal and age‐dependent manner, starting from small vessel wall damage (stage 1A), proceeding to  CBF  reduction (stage 1B), non‐occlusive (stage 2), and finally, occlusive thrombi (stage 3). Wistar animals also demonstrated small vessel wall damage, but were free of any of the later  HA  stages. Nearly half of all  SHRSP  additionally displayed vascular Methoxy‐X04 positivity indicative of cortical  CAA . Vascular β‐amyloid deposits were found in small vessels characterized by thrombotic occlusions (stage 2 or 3). Post‐mortem analysis of the rat brains confirmed the findings derived from intravital 2 PM  microscopy. Our data thus overall suggest that advanced  HA  may play a role in  CAA  development with the two small vessel disease entities might be related to the same pathological spectrum of the aging brain.

The association between hypertensive arteriopathy and cerebral amyloid angiopathy in spontaneously hypertensive stroke‐prone rats