Grants awarded through this RFA were intended to advance our understanding of the genetic basis of autism, and in particular the potential role of missense and in-frame deletion variants in conferring risk. Investigators who are interested in developing medium- or high-throughput screens to test the functional effects of missense and in-frame deletion variants identified in the Simons Simplex Collection (SSC) and other autism collections were encouraged to apply.

Grants awarded through this RFA were intended to advance our understanding of the impact of activation of the innate immune system on behavioral, circuit, synaptic and neuronal functions in order to understand the consequences of infection and immune activation on autism-related behaviors. Experiments were expected to include physiologically relevant activation/inhibition of the innate immune system in animal models of autism and to focus on neuronal, synaptic and circuit function.

This RFA was intended to advance our understanding of the circuit basis for behavioral and cognitive alterations relevant to autism spectrum disorders (ASD). The goal was to determine the downstream consequences of autism-associated genetic perturbations on neural circuitry, with an emphasis on how collections of neurons operate in concert during autism-relevant behaviors.

This RFA sought proposals that take advantage of the unique combination of biospecimens and rich phenotypic information collected by Simons VIP. Although SFARI was open to many different approaches, we gave priority to those that aim to accomplish a comprehensive characterization of RNA expression differences and correlate such expression patterns with phenotypes. Furthering the ability to include genomic analysis was considered be an additional strength. The data produced in this effort was later made available to the research community.

This RFA sought proposals that aimed to comprehensively analyze the behavior of mouse models that have been generated with targeted genetic mutations based on strong human genetic evidence implicating them in autism spectrum disorders. We expected investigators to test at least three genetic models in the same background strain (C57BL/6). In addition, investigators needed to analyze the behavior of one of the selected autism mouse models in a different genetic background, such as a hybrid background from two inbred strains