Deficits in brain cells’ homeostasis and metabolism are suspected to occur ahead of the atrophy observed throughout the brain of AD patients with potential interactions between Amyloid/Tau deposits and the Na/K-pump activity leading to increased cerebral sodium concentrations. Yet this increase remains to be confirmed. We present a multimodal imaging study combining structural 1H-MRI, quantitative 23Na MRI at 7T in association with Tau- and Amyloid-PET. We show that total sodium concentration is increased in multiple brain regions in AD compared to cognitively healthy controls, and that these changes are more strongly correlated with local Tau- than Amyloid-loads.
This abstract and the presentation materials are available to members only; a login is required.