Large artery stiffness is a frequent condition that arises with ageing, and is accelerated by the presence of co-morbidities like hypertension, obesity and diabetes. Although epidemiological studies have indicated an association between arterial stiffness, cognitive impairment and dementia, the precise effects of stiff arteries on the brain remains obscure. This is because, in humans, arterial stiffness is often accompanied by other factors such as age, high blood pressure, atherosclerosis and inflammation, which could themselves damage the brain independently of stiffness. Therefore, the question remains: is arterial stiffness a true risk for cognitive decline?Or, is it a confounding factor? In this review, we provide an overview of arterial stiffness and its impact on brain function based on human and animal studies. We summarize the evidence linking arterial stiffness to cognitive dysfunction and dementia, and discuss the role of new animal models to better understand the mechanisms by which arterial stiffness affects the brain. We close with an overview of treatments to correct stiffness and discuss the challenges to translate them to real patient care.

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Background: Vascular risk factors such as arterial stiffness play an important role in the etiology of Alzheimer’s disease (AD), presumably due to the emergence of white matter lesions. However, the impact of arterial stiffness to white matter structure involved in the etiology of AD, including the corpus callosum remains poorly understood. Objective: The aims of the study are to better understand the relationship between arterial stiffness, white matter microstructure, and perfusion of the corpus callosum in older adults. Methods: Arterial stiffness was estimated using the gold standard measure of carotid-femoral pulse wave velocity (cfPWV). Cognitive performance was evaluated with the Trail Making Test part B-A. Neurite orientation dispersion and density imaging was used to obtain microstructural information such as neurite density and extracellular water diffusion. The cerebral blood flow was estimated using arterial spin labelling. Results: cfPWV better predicts the microstructural integrity of the corpus callosum when compared with other index of vascular aging (the augmentation index, the systolic blood pressure, and the pulse pressure). In particular, significant associations were found between the cfPWV, an alteration of the extracellular water diffusion, and a neuronal density increase in the body of the corpus callosum which was also correlated with the performance in cognitive flexibility. Conclusion: Our results suggest that arterial stiffness is associated with an alteration of brain integrity which impacts cognitive function in older adults.

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Hypertension, elevated morning blood pressure (BP) surges, and circadian BP variability constitute risk factors for cerebrovascular events. Nevertheless, while evidence indicates that hypertension is associated with cognitive dysfunctions, the link between BP variability and cognitive performance during aging is not clear. The purpose of this study is to determine the interaction between relative morning BP, cerebral blood flow (CBF) levels, and cognitive performance in hypertensive older adults with controlled BP under antihypertensive treatment. Eighty-four participants aged between 60 and 75 years old were separated into normotensive (n=51) and hypertensive (n=33) groups and underwent 24-hour ambulatory BP monitoring. They were also examined for CBF in the gray matter (CBF-GM) by magnetic resonance imaging and 5 cognitive domains: global cognition, working memory, episodic memory, processing speed, and executive functions. There was no difference in cognitive performance and CBF between normotensive and controlled hypertensive participants. Through a sensitivity analysis, we identified that, among relative morning BP variables, the best fit for CBF values in this cohort was the morning-evening difference in BP. The relative morning BP was negatively associated with CBF-GM in these hypertensive older adults only. In turn, CBF-GM levels were negatively associated with working and episodic memory scores in hypertensive older adults. This is the first extended study demonstrating an association between high relative morning BP and lower levels of CBF-GM, including the further impact of CBF-GM levels on the cognitive performance of specific domains in a community-based cohort of older adults with hypertension.

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