Project aim: Identifying changes in neuronal communication occurring in aging and Alzheimer's disease when associated with pain comorbidities.
Beyond memory deficits other behavioral symptoms of Alzheimer's disease, less well characterized but frequent, are apathy, anxiety, restlessness and irritability. These impairments in social interaction and personality are particularly debilitating and remain difficult to treat because the biological mechanisms underlying them remain unknown. Although the expression of molecular markers of disease, such as Aβ or phosphorylation of tau protein increases with age, their direct association with these behavioral alterations still remains unclear. Recently we demonstrated that alterations in the basal synaptic activity in the prefrontal cortex correlates with changes in social behavior observed in a transgenic mouse model of Alzheimer's disease.
We now aim to save in long term changes in neuronal activity of the prefrontal cortex, in vivo, in control mice and a model of Alzheimer's disease, when they execute behavioral tasks, targeted to assess their social interactions. Thereafter, based on electrophysiological results and their behavioral correlates, we will manipulate neuronal activity in the regions identified in order to restore, in whole or in part, the social behavior of animals with deficits. To modulate in real time the neural activity of animals not anesthetized and freely interacting, we will benefit from a single system developed in collaboration with the Faculty of Engineering of Laval University, that combines both wireless electrophysiological recordings and the optical stimulation.