Lieu: Brunoy (+ visio)

AbstractAlzheimer's disease is linked to the cerebral accumulation of aggregated amyloid-β (Aβ) peptides that initiate a pathological cascade leading to fibrillar aggregation of tau protein, tau spreading and leading to synaptic alterations. Mouse lemurs have been proposed as model of Alzheimer's disease… but what did we learn on the disease from these animals? First, evaluation of normal aging processes, showed that amyloid deposits and to a lesser extent, tau lesions can spontaneously occur in primates. This is logical given the similarity between amyloid and tau sequences in humans and mouse lemurs. However Alzheimer' disease cannot be considered as occurring in mouse lemurs. Mouse lemurs can display spontaneously occurring cerebral atrophy. This atrophy can be partly linked to amyloid lesions, but is probably more associated with alteration of glucose metabolisms. Then we could learn that amyloid and tau lesions can be transmissible in a primate. These proteins thus behave like prions. Their transmissions leads to neuronal loss, cerebral atrophy, functional impairments, and cognitive changes, which suggests caution with the manipulation of such proteins. Finally, we learn that the transmission of Alzheimer pathology leads to a reorganization of cerebral transcriptome affecting microglia cells. The organization of these cells is very different in rodents and primates, which make the lemur very useful to understand microglial changes induces by these proteins.