Cross-Species Studies of ASD — Request for Applications

The Cross-Species Studies of ASD request for applications (RFA) supported research on ASD-relevant behaviors and their underlying neurobiological mechanisms conducted in parallel across human and non-human animals. Because the focus was on translation across species, in addition to being relevant to ASD, the behaviors under study needed to be conserved across species and able to be measured objectively and quantitatively. Three domains SFARI recognized as fitting these criteria included sensory function, motor function and sleep, although other behaviors were considered if there was a strong argument that they met these criteria. All three of these domains are recognized as being affected in many people with ASD, with sensory atypicalities now included in the DSM-5 diagnostic criteria for autism. Competitive applications not only studied the same general behavioral domains in humans and non-human animals, but were able to measure truly analogous behaviors in humans and model animals, e.g., by aligning the tasks used and/or tapping into a shared computational construct in both species.

Beyond measuring behaviors in parallel across species, special emphasis was placed on furthering our understanding of the underlying neurobiological mechanisms with an eye towards developing novel biomarkers or interventions. Therefore, behaviors for which there is evidence of evolutionary conservation of such mechanisms, e.g., at the circuit level, were prioritized. Studies in animals were expected to take advantage of the use of more invasive techniques that would not be possible in humans, yet attempt to link findings from such techniques with analogous measurements in humans, e.g., LFP/EEG, or mesoscale Ca2+ imaging/fMRI.

In addition to aligning measurements of behavior and circuit function across species, this RFA encouraged applicants to carefully consider other traits of their study subjects, both human and non-human species, including age, sex and genotype or genetic background. While there is no rigorous way to model “idiopathic” ASD in non-human animals, we encouraged applicants to carefully consider and rationalize comparisons of humans with idiopathic and/or known genetic causes of ASD with genetically modified animal models.