The synaptic connections between brain cells have a remarkable capacity for activity-dependent plasticity that is critical for learning and memory storage. Such plasticity is routinely impaired in animal models of a host of neurological diseases. While the molecular mechanisms of plasticity are not yet fully understood, molecules already known to support or enhance plasticity are being targeted for treating diseases characterised by memory deficits.

This talk will review our collaborative research related to these topics, with a focus on soluble amyloid precursor protein-alpha.