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Abstract #3162

Can familial Alzheimer variability affect brain networks? Exploration through Osaka Ab variant inoculation in mice.

Marina Celestine1, Jean-Baptiste Pérot1, Muriel Jacquier-sarlin2, Karine Cambon1, Julien Flament1, Alain Buisson2, Anne-Sophie Hérard1, and Marc Dhenain1
1Université Paris-Saclay, Commissariat à l’Energie Atomique et aux Energies Alternatives (CEA), Centre National de la Recherche Scientifique (CNRS), Molecular Imaging Research Center (MIRCen), Laboratoire des Maladies Neurodégénératives, Fontenay-aux-roses, France, 2University Grenoble Alpes, Inserm, U1216, Grenoble Institut Neurosciences (GIN), Grenoble, France

Early brain dysfunctions found in Alzheimer's disease are due to soluble pathological forms of b-amyloid peptide (Aβ). Among the familial Aβ mutations, the Osaka-Aβ variant is characterized by the intraneuronal accumulation of toxic Aβ without forming extracellular Aβ deposition. It affects synaptic function by modulating excitatory pathways leading to memory defects. Here, we performed a multimodal study to unveil brain network signatures of the pathology. Combining resting-state fMRI, gluCEST and diffusion analysis, we revealed that exposition to Osaka-Aβ leads to abnormal brain connectivity through impairment of the default mode and the hippocampal-memory networks.

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