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.

Studying interactions between older children and adolescents with their adult caregivers is an important indicator of communication skills and are especially important for assessing children with ASD. Mark Clements aims to develop a fully automated audio recording tool for use in assessing communication skills in children with ASD in naturalistic (e.g., home) environments.

Genetic risks for autism are diverse and encompass mutations and copy number variations in hundreds of genes. However, autism is diagnosed through the evaluation of a shared set of symptoms that include social interaction deficits and repetitive or restrictive behaviors.

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.

Motor dysfunction is common in autism. The primary motor cortex (area M1) has been implicated in the manifestation of these symptoms. Stelios Smirnakis proposes to study M1 circuit function, particularly during motor skill learning, to elucidate mechanisms that underlie motor deficits in autism.

Somatic mosaicism, or the emergence of variations in the sequence or structure of the genome of somatic cells, has been detected in both healthy individuals and individuals with various diseases, particularly cancer. It has been suggested that somatic variations play a major role in driving neuronal diversity and genome evolution. However, the extent to which mosaicism occurs in normal development, and its significance in brain disorders, has only recently begun to be investigated.

Over the past few years, the number of genes associated with autism spectrum disorder (ASD) has increased substantially. More than 65 genes are strongly associated with autism, and current estimates suggest that hundreds of genes may play a role.

Both genetic and environmental factors contribute to the development of autism spectrum disorder (ASD). Maternal inflammation during pregnancy is known to increase the risk of ASD and other neuropsychiatric disorders in offspring, but the mechanism by which this occurs is still poorly understood. For example, it is currently unknown whether the gut microbiota composition in the mother during pregnancy influences the inflammation associated with ASD or if microbe-regulated immune responses are translated into effectors of ASD phenotypes in the offspring.

One hallmark of several autism spectrum disorders (ASDs) is altered protein synthesis in the brain, which results in synaptic dysfunction and disease pathology. Genetic variations in PTEN, TSC1, TSC2, FMR1, SHANK3 and NLGN3, and microdeletions at 16p11.2 have all been linked to ASDs, and mouse models of these mutations exhibit alterations in a form of synaptic plasticity called metabotropic glutamate receptor-induced long-term depression (mGluR-LTD). Many studies support a role for mGluR-LTD in learning, with alterations in mGluR-LTD linked to a variety of neurological disease states, including ASDs. These studies have also demonstrated that the proper functioning of mGluR-LTD relies on rapid synthesis of proteins, leading to the suggestion that aberrations in mRNA translation may contribute to disease pathology. However, it remains unclear what particular mRNAs are involved in this process.