Project: Alzheimer's disease (AD)

About

Amyloid precursor protein (APP) is a key protein involved in the etiology of AD. This protein is cleaved into several fragments by a highly regulated process. Little is known about the physiological function of APP and its fragments. The most studied fragment, amyloid b (Ab), has been shown to disrupt neuronal plasticity and associated behaviors, especially in brain areas involved in memory formation such as the hippocampus. However, several other peptides derived from APP cleavage likely regulate brain function under physiological conditions. The main goal of our research is to better understand the physiological role of Ab and these other APP-derived peptides in the brain. Identifying their endogenous function should provide insight into how dysregulation of APP cleavage or degradation of these peptides in the brain contribute to the onset of AD. In collaboration with computational neuroscience experts, we are working on modeling synaptic disruptions in these pathological conditions to better understand the impact of these APP fragments on hippocampal neurons at the level of the individual neuron and in the context of a neuronal network.