Abstract #2594

Ultra-High Field Sodium MRI in Alzheimer’s Disease Reveals Stage-dependent Metabolic Alterations Associated with Tau-pathology

Alexa Haeger^1,2,3, Michel Bottlaender^1,4, Julien Lagarde^4,5,6, Renata Porciuncula Baptista¹, Cécile Rabrait-Lerman¹, Volker Luecken^2,3, Jörg Bernhard Schulz^2,3, Alexandre Vignaud¹, Marie Sarazin^4,5,6, Kathrin Reetz^2,3, Sandro Romanzetti^2,3, and Fawzi Boumezbeur¹

¹BAOBAB, CNRS, Paris-Saclay University, CEA-NeuroSpin, Gif-sur-Yvette, France, ²Department of Neurology, RWTH Aachen University, Aachen, Germany, ³JARA-BRAIN Institute of Molecular Neuroscience and Neuroimaging, Forschungszentrum Jülich GmbH, Julich, Germany, ⁴BioMaps, CNRS, Inserm, Paris-Saclay University, CEA-SHFJ, Orsay, France, ⁵Neurology of Memory and Language, GHU Paris Psychiatrie & Neurosciences, Sainte-Anne Hospital, Paris, France, ⁶Université de Paris, Paris, France

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.

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