Timothy Roberts and his colleagues at the Children’s Hospital of Philadelphia are studying the responsiveness of neural oscillatory measures to acute administration of STX209 (arbaclofen), a GABAB agonist and a candidate therapeutic for autism spectrum disorder (ASD).

It is well established that homeostatic signaling systems interface with the mechanisms of developmental and learning-related plasticity to achieve stable yet flexible neural function and animal behavior. Experimental evidence from organisms as diverse as Drosophila, mice and humans demonstrates that homeostatic signaling systems stabilize neural function through the modulation of synaptic transmission, ion channel abundance and neurotransmitter receptor trafficking. At a fundamental level, if homeostatic plasticity is compromised, the nervous system is likely to be more sensitive to perturbations. Graeme Davis and his colleagues speculate that impaired homeostatic plasticity could contribute to autism by making the developing nervous system vulnerable to perturbations of any origin, including genetic, environmental or immunological stresses.

Whole-exome sequencing studies of sporadic autism cases have identified SCN2A, which encodes the neuronal voltage-gated sodium channel NaV1.2, as one of the most commonly mutated genes associated with autism. How dysfunctional NaV1.2 affects neurons and consequent circuit function to produce behaviors associated with autism is not well understood.

Fei Xu and her colleagues conduct research on early cognitive and language development in typically developing infants and children. Using a novel approach of conceptualizing autism as a learning disorder, the researchers aim to investigate the capacity of children with autism in making inductive generalizations.

Although mutations — the fundamental process by which genomic variation is acquired — are necessary to the evolution and success of a species, they are also the origin of all genetic disease. Hence, defining the mechanisms that control their occurrence is crucial to our basic understanding of genome biology, disease mechanisms and, ultimately, evolution.

Anatomical and electrophysiological studies have made it clear that dysfunction in the cerebellum, and in Purkinje cells specifically, is linked to behavioral abnormalities in autism. This correlation is compelling, but it has been difficult to make a causative link between the anatomical and physiological defects and the associated behaviors.

Although autism is characterized primarily by impairments in social skills and communication, as well as restricted interests and repetitive behaviors, it has become evident that attention abnormalities may play a critical role in the symptom presentation of the disorder. Attention refers to the activity of a set of alerting, orienting and executive-control brain networks. Flexibility in these networks allocates mental resources to influence the priority of domain-specific information processing. By using the Attention Network Test (ANT), Jin Fan and his colleagues at theQueens College/CUNY previously showed lower efficiency of the visual alerting and executive control networks in autism, when compared with controls.

Multiple autism spectrum disorders share similar neuronal deficits at the molecular and cellular levels. Understanding the mechanism underlying those deficits helps researchers identify valuable targets for therapeutic development.