Autism is comprised of a clinically heterogeneous group of disorders, collectively termed 'autism spectrum disorders,' that share common features. Only an estimated 10 to 15 percent of autism cases are monogenic - caused by mutation in a single gene - but the molecular alterations in these disorders could reveal common pathogenic pathways shared by others across the spectrum. Studies of many of the mutations linked to autism in humans point to disrupted activity of synapses - the junctions between neurons - and altered synthesis of synaptic proteins. In particular, the levels of proteins related to the ability of a synapse to change in strength, termed 'plasticity,' seem to be altered in people with autism. The corresponding changes in network connectivity and performance may produce cognitive impairment. Mutations in monogenic disorders with high co-incidence with autism could lead to excessive or dysregulated synaptic protein synthesis, which may be one mechanism contributing to autism in humans. Peng Jin and Junmin Peng at Emory University have developed high-throughput proteomic analysis using metabolically labeled mice, providing an opportunity to systematically examine synaptic protein synthesis. They plan to compare the alterations of synaptic protein synthesis in various mouse models of autism-linked monogenic disorders, to determine whether there are any common alterations. Restoring normal expression of these synaptic proteins could become a promising therapeutic strategy for treating autism, and perhaps mental retardation as well.