Key result
Angiotensin II treatment for 28 days increased arterial stiffness but did not further impair visuospatial learning, memory, or cerebral amyloid load in Alzheimer's disease mouse models.
Why the study?
Evidence suggests a mechanistic link between arterial stiffness, hypertension, and Alzheimer's disease, but whether pharmacologically inducing arterial stiffness and hypertension impairs Alzheimer's disease progression required investigation.
Does pharmacological induction of arterial stiffness and hypertension with angiotensin II impair the progression of Alzheimer's disease in murine models?
Does pharmacological induction of arterial stiffness and hypertension with angiotensin II impair the progression of Alzheimer's disease in murine models?
Short-term induction of hypertension and arterial stiffness with angiotensin II does not acutely worsen cognitive function or amyloid pathology in Alzheimer's disease mouse models.
Ang II-induced stiffness does not worsen cognition or amyloid in AD mice; leaves open vascular contributions to human Alzheimer's.
Given the unprecedented rise in the world’s population, the prevalence of prominent age-related disorders, like cardiovascular disease and dementia, will further increase. Recent experimental and epidemiological evidence suggests a mechanistic overlap between cardiovascular disease and dementia with a specific focus on the linkage between arterial stiffness, a strong independent predictor of cardiovascular disease, and/or hypertension with Alzheimer’s disease. In the present study, we investigated whether pharmacological induction of arterial stiffness and hypertension with angiotensin II (1 µg·kg−1·min−1 for 28 days via an osmotic minipump) impairs the progression of Alzheimer’s disease in two mouse models (hAPP23+/− and hAPPswe/PSEN1dE9 mice). Our results show increased arterial stiffness in vivo and hypertension in addition to cardiac hypertrophy after angiotensin II treatment. However, visuospatial learning and memory and pathological cerebral amyloid load in both Alzheimer’s disease mouse models were not further impaired. It is likely that the 28-day treatment period with angiotensin II was too short to observe additional effects on cognition and cerebral pathology.
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Hendrickx et al. (2022) studied Alzheimer's disease (mouse models). Angiotensin II was evaluated on visuospatial learning and memory and pathological cerebral amyloid load. Angiotensin II treatment for 28 days increased arterial stiffness but did not further impair visuospatial learning, memory, or cerebral amyloid load in Alzheimer's disease mouse models.
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