Autism spectrum disorder (ASD) is seen as a collection of disorders that is predominantly developmental in nature and largely genetic in origin. However, there is tentative evidence to support the idea that fever can improve symptoms in individuals with ASD, which suggests that behavioral symptoms could improve transiently under certain conditions. This implies that the circuits affected in ASD possess the structural integrity to perform relatively normally under certain conditions. Fever could conceivably improve brain function in ASD through elevated body and brain temperature. Alternatively, changes to brain function may be a result of the inflammatory response that underpins fever.

The Simons Initiative for the Developing Brain was established in 2017 and is directed by Peter Kind. It is a collaborative venture between researchers at the University of Edinburgh and it aims to build on the existing fundamental and clinical strengths in molecular, cellular, circuit and behavioral neuroscience located with the Patrick Wild Center to elucidate biological mechanisms underlying autism and to use this information to deliver rational therapeutic interventions.

Most individuals with autism experience at least one form of hypersensitivity from the five senses. These alterations in sensory-related behaviors can lead to profound limitations on an individual’s ability to work, interact with family and participate in leisure activities. Furthermore, these atypical responses to otherwise normal sensory stimuli may be closely associated with the core symptoms of autism, such as social deficits and repetitive behaviors. Despite the importance of sensory abnormalities in the pathogenesis of autism, how the brains of individuals with autism receive information from the five senses at the subcortical level and how such information becomes transformed into aversive responses has not been investigated.

Perseverance on sameness is a core feature of autism. Kwan aims to combine state-of-the-art optical imaging and behavioral methods to test the possibility that perturbed learning-related activity may underlie inflexible behavior in an ASD mouse model.

Autism spectrum disorders (ASDs) encompass a number of disorders that are typified by communication deficits, reduced behavioral flexibility, poor socialization, learning disabilities and a tendency toward repetitive behaviors. While the pathophysiology underlying ASDs remains largely unknown, the recent identification of gene mutations associated with ASDs has significantly advanced our understanding of these disorders. Many gene mutations found in ASDs have been shown to affect the formation, functional efficacy and plasticity of both excitatory and inhibitory synapses. Hence, a hypothesis of an imbalanced neuronal excitation and inhibition has been put forward as an underlying cause of ASDs.

Autism is a neurodevelopmental disorder, and sensorimotor disturbances are among the earliest signs of atypical development in autism, revealing themselves in early infancy. As every parent knows, infants spend most of their time asleep, and about half of that sleep time is spent in rapid eye movement (REM) sleep. One of the defining features of REM sleep is myoclonic twitching, a phenomenon which is thought to play a critical role in sensorimotor development. Twitching — jerky movements of the limbs, head, face and eyes — occurs abundantly and exclusively during REM sleep, with sensory feedback from twitching limbs acting as a primary driver of neural activity throughout the sensorimotor system. This suggests that twitching plays a role in shaping, tuning, and mapping the developing sensorimotor system and that alterations in twitching might serve as a useful model for tracking sensorimotor disturbances in autism.

Neuroimaging studies have described altered structural and functional connectivity across brain regions of individuals with autism spectrum disorder (ASD). These findings have led to the hypothesis that altered brain connectivity may provide a key pathophysiological contribution in ASD. However the neurobiological determinants and significance of these findings remain unclear.

Hundreds of susceptibility genes have been identified for autism spectrum disorder (ASD), and many are related to synaptic function. This has led to a hypothesis that the deficits in ASD may reflect an imbalance in the relative contributions of excitatory and inhibitory synaptic inputs. Canonical neural computations are stereotyped, modular circuit functions that occur across the brain and can provide building blocks for more complex operations. Disruptions to these computations would be expected to have negative behavioral consequences. Interestingly, divisive normalization, one such canonical neural computation, computes a ratio between individual neuronal responses and the summed population activity, and inherently reflects the balance of excitation to inhibition.

Autism spectrum disorders (ASDs) represent a group of neurodevelopmental disorders for which the underlying etiologies are heterogeneous. Risk factors range from environmental insults to single gene mutations. A unifying model explaining how this array of risk factors leads to deficits in communication, social interactions, and sensory and repetitive behavior is lacking.