Autism Lights the Way from Genetics and Neural Computation to the Twenty-First-Century Science of Human Cognitive Diversity

Discoveries in autism research, as in all scientific endeavours, are determined not just by the data that we scientists observe but by the questions that we ask.  Empirical science is inseparable from such rhetorical scaffolding, which simultaneously supports and limits both the data that we decide to collect and the interpretations that we impose on these data.  It's natural for us to demand:  What is autism's biological basis?  What are the genes that cause autism?  What distinguishes autistic brains and autistic cognition from typical brains and typical cognition? Implicit in this rhetoric are the assumptions that autism has a singular biological basis, that autism susceptibility is conferred by individual genetic variants, and that autistic neural and congitive processes differ 
categorically from typical ones.  These assumptions make sense within a twentieth-century scientific frame in which singular causal factors (single genes, focal brain lesions, circumscribed cognitive deficits) manifest as disease states that are unitary and entirely distinct from healthy states, and in which contributing factors are monotonic in their relation to disease outcome and linear in their interactions with each other.  An accumulation of evidence points, rather, to autism as a nonlinear, network-level 
perturbation of the same developmental processes that underlie normal human 
cognitive diversity.  Thus the more closely we examine autism, the more we find ourselves staring into a mirror.