University of Tasmania, Australia

The project aims to define the direct effect of sensory deprivation on properties of target neurons, in terms of their excitability, reorganisation of circuitry and their processing of APP. The results will give new insight into the initiating processes of Aβ aggregation. We will establish whether modulation of sensory input is an effective treatment therapy post initiation of Aβ aggregation. The project employs both in vivo and in vitro techniques, including electrophysiology. Currently the majority of AD therapies target Aβ aggregation and accumulation but none of them have been shown to be effective in pivotal phase III therapeutic trials. One can argue that the failure of anti-Aβ therapy in patients with clinically diagnosed AD may be due to the considerable accumulation of neurotoxic Aβ over a protracted period. Hence it is relevant to develop a therapy that is effective in prevention rather than a treatment setting. In this regard, this project, which will lead to better understanding of mechanisms regulating AD pathogenesis, will make a significant contribution towards the future development of a protective measure against AD.