Humans seem to have developed dedicated systems for detecting the prototypical gait of moving animals. One paradigm for operationalizing this ability is a point light display, which simulates animals moving in the dark with just a few lights on their joints.
We are able to classify these sparse moving points as biological motion and can often even make inferences about the characteristics of the moving agent. See for yourself in this 31 s video:
Previous studies have indicated that toddlers with autism have deficits in perceiving biological motion. This is not surprising, because social information is embedded within the stimuli.
Kaiser et al took this further by using this point light display paradigm and fMRI on 1) children with ASD, 2) siblings of children with ASD, and 3) control children.
They looked for regions differentially activated between biological light displays and scrambled light displays. They then compared the degree of differential neural activity between groups.
Brain regions were classified as having 1) less differential activation in ASD children in biological conditions as compared to siblings and controls (orange below), 2) less differential activation in ASD children and siblings as compared to controls (yellow), 3) enhanced differential activation in siblings (green), or 4) no statistically significant difference in differential activation between groups (uncolored).
Their approach helps tease out the neural circuits underlying why some individuals with genetic risk factors don’t develop ASD. The two main brain regions they implicated were the vmPFC (of emotional decision making fame) and the right posterior STS. Could we imagine some study attempting to stimulate these regions in a model of ASD to mimic the development of compensatory mechanisms?