Hypertension accelerates cerebral tissue PO2 disruption in Alzheimer's disease. (10th January 2020)

• Record Type: Journal Article
• Authors: Lu, Xuecong; Moeini, Mohammad; Li, Baoqiang; Thorin, Éric; Lesage, Frédéric
• Is Part Of: Neuroscience letters. Volume 715(2020)
• Publication Date: 2020-01-10
• Subjects: Alzheimer's disease -- Cerebral tissue oxygenation -- Stimulation -- Hypertension -- Exercise -- Two-photon microscopy; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2019.134626
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: During rest periods, cerebral tissue PO2 values close to the arteriolar wall were lower in the AD groups. The PO2 spatial decay as a function of distance to arteriole was increased by hypertension. During stimulation, tissue PO2 response had a similar spatial dependence across groups. Post-stimulation dynamics of tissue PO2 was larger in AD groups than in the controls. Some of these changes were reversed by exercises in AD mice. Abstract: This study measured stimulus-evoked brain tissue oxygenation changes in a mouse model of Alzheimer disease (AD) and further explored the influence of exercise and angiotensin II-induced hypertension on these changes. in vivo two-photon phosphorescence lifetime microscopy was used to investigate local changes in brain tissue oxygenation following whisker stimulation. During rest periods, PO2 values close to the arteriolar wall were lower in the AD groups and the PO2 spatial decay as a function of distance to arteriole was increased by hypertension. During stimulation, tissue PO2 response had a similar spatial dependence across groups. Tissue PO2 response in post-stimulation period was larger in AD groups (e.g., AD6 and ADH6) than in the controls (WT6 and WTH6). After a 3-month voluntary exercise period, some of these changes were reversed in AD mice. This provides novel insight into tissue oxygen delivery and the impact of blood pressure control and exercise on brain tissue oxygenation in AD.