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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