Abstract
This study aims to assess the impact of unilateral increases in carotid stiffness on cortical functional connectivity measures in the resting state. Using a novel animal model of induced arterial stiffness combined with optical intrinsic signals and laser speckle imaging, resting state functional networks derived from hemodynamic signals are investigated for their modulation by isolated changes in stiffness of the right common carotid artery. By means of seed-based analysis, results showed a decreasing trend of homologous correlation in the motor and cingulate cortices. Furthermore, a graph analysis indicated a randomization of the cortex functional networks, suggesting a loss of connectivity, more specifically in the motor cortex lateral to the treated carotid, which however did not translate in differentiated metabolic activity.
Highlights
Arterial hypertension is a non-communicable disease with prevalence between 25% and 30% of the world adult population [1] and is a risk factor in early brain aging, the development of cognitive dysfunctions and dementias
Imaging correlates of aging and age-induced cognitive deficits include a decrease in connectivity and efficiency of functional brain networks [8], smaller brain volume and weight [9,10] and a reduction in cerebral blood flow (CBF) [11,12] related to endothelial dysfunction [13,14]
Using a new carotid calcification murine model, we were able for the first time to investigate the isolated effect of unilateral carotid stiffness on resting state networks
Summary
Arterial hypertension is a non-communicable disease with prevalence between 25% and 30% of the world adult population [1] and is a risk factor in early brain aging, the development of cognitive dysfunctions and dementias. Hardening of the arteries has been identified as a risk factor in the development of cardiovascular disease (CVD) and may play a role in the development of such deficits. Arterial stiffness has been shown to be a predictor of cognitive decline and dementia [6]. Basic cognitive functions such as attention and memory are adversely affected by aging [7], a process accelerated by risk factors for CVD. A key step forward is to understand the impact of systemic physiology and vascular hardening and/or stenosis on functional imaging brain signals derived from hemodynamics
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