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The exponential rise in autism diagnosis, paired with the high heterogeneity of the newly diagnosed children, call for diversification of therapies that currently treat autism under a one-size-fits-all model. Through several surveys involving practitioners from top therapies of autism, we find that there is awareness of the need to bring transformative changes to the curricula of accreditation systems guided by science of the mid-20th Century. Furthermore, we find enthusiasm for combining principles of neuroscience and wearable biosensors to capture nuance aspects of behavior that currently escape the naked eye. Despite boasting different philosophies, each of the groups surveyed acknowledges the relevance of approaches complementary to their own and the need for a new collaborative model. This work shows that the time is ripe for an autism renaissance and that the change will likely come from within these therapists and service providers themselves.

The brain integrates streams of sensory input and builds accurate predictions, while arriving at stable percepts under disparate time scales. This stochastic process bears different unfolding dynamics for different people, yet statistical learning (SL) currently averages out, as noise, individual fluctuations in data streams registered from the brain as the person learns. We here adopt a new analytical approach that instead of averaging out fluctuations in continuous electroencephalographic (EEG)-based data streams, takes these gross data as the important signals. Our new approach reassesses how individuals dynamically learn predictive information in stable and unstable environments. We find neural correlates for two types of learners in a visuomotor task: narrow-variance learners, who retain explicit knowledge of the regularity embedded in the stimuli. They seem to use an error-correction strategy steadily present in both stable and unstable environments. This strategy can be captured by current optimization-based computational frameworks. In contrast, broad-variance learners emerge only in the unstable environment. Local analyses of the moment-by-moment fluctuations, naïve to the overall outcome, reveal an initial period of memoryless learning, well characterized by a continuous gamma process starting out exponentially distributed whereby all future events are equally probable, with high signal (mean) to noise (variance) ratio. The empirically derived continuous Gamma process smoothly converges to predictive Gaussian signatures comparable to those observed for the error-corrective mode that is captured by current optimization-driven computational models. We coin this initially seemingly purposeless stage exploratory. Globally, we examine a posteriori the fluctuations in distributions’ shapes over the empirically estimated stochastic signatures. We then confirm that the exploratory mode of those learners, free of expectation, random and memoryless, but with high signal, precedes the acquisition of the error-correction mode boasting smooth transition from exponential to symmetric distributions’ shapes. This early naïve phase of the learning process has been overlooked by current models driven by expected, predictive information and error-based learning. Our work demonstrates that (statistical) learning is a highly dynamic and stochastic process, unfolding at different time scales, and evolving distinct learning strategies on demand.

The advent of open access to genomic data offers new opportunities to revisit old clinical debates while approaching them from a different angle. We examine anew the question of whether psychiatric and neurological disorders are different from each other by assessing the pool of genes associated with disorders that are understood as psychiatric or as neurological. We do so in the context of transcriptome data tracked as human embryonic stem cells differentiate and become neurons. Building upon probabilistic layers of increasing complexity, we describe the dynamics and stochastic trajectories of the full transcriptome and the embedded genes associated with psychiatric and/or neurological disorders. From marginal distributions of a gene’s expression across hundreds of cells, to joint interactions taken globally to determine degree of pairwise dependency, to networks derived from probabilistic graphs along maximal spanning trees, we have discovered two fundamentally different classes of genes underlying these disorders and differentiating them. One class of genes boasts higher variability in expression and lower dependencies (“active genes”); the other has lower variability and higher dependencies (“lazy genes”). They give rise to different network architectures and different transitional states. Active genes have large hubs and a fragile topology, whereas lazy genes show more distributed code during the maturation toward neuronal state. Lazy genes boost differentiation between psychiatric and neurological disorders also at the level of tissue across the brain, spinal cord, and glands. These genes, with their low variability and asynchronous ON/OFF states that have been treated as gross data and excluded from traditional analyses, are helping us settle this old argument at more than one level of inquiry.