Autism Spectrum Disorders (ASD) are characterised by impaired communication and social behaviours. ASD-associated mutations occur in the Shank family of synaptic proteins, and we have shown that these mutations weaken synapse function in the brain. Interestingly, zinc enhances Shank function, and our recent data show that increasing dietary zinc reverses ASD-associated behaviours in Shank3 ASD mice. We therefore hypothesise that Shank proteins form part of a zinc-dependent synaptic signalling pathway that could be at the heart of a treatment strategy for ASD. We have created a multidisciplinary international team with expertise in synaptic physiology, behavioural neuroscience, and microbiology that will enable us to (1) identify the mechanisms underlying this dietary zinc-induced treatment, and (2) to determine the breadth of the applicability of zinc treatment to other ASD mutations. Together, our data will provide a complete characterisation, from synapse to behaviour, of the impact and potential of dietary zinc in ASD.