Alzheimer disease (AD) is associated with an abnormal brain activity common to other brain disorders such as epilepsy, Down syndrome, autism and frontotemporal dementia. Growing number of evidence indicates that during early stages of AD an imbalance between synaptic excitation and inhibition occurs resulting in cortical and hippocampal overexcitation. While this aberrant hyperactivity may emerge from several mechanisms, recent evidence points to a disruption in GABAA-mediated transmission. Hence, the objective of this project is to test whether several AD-related symptoms can be prevented or attenuated by reversing the deficits in GABAA-mediated inhibition in AD.
In vivo optogenetics; in vivo wireless electrophysiology; in-vivo micro-optrode recordings; cognitive and social behavioral measurments; immunoblots; immunostainings; confocal microscopy; Lucifer yellow injections; neurons morphology reconstruction