Mice that lack the autism- and schizophrenia-linked gene MEF2C in cortical neurons have an imbalance of excitatory and inhibitory synapses, and impaired social and cognitive abilities.

Newly identified gain-of-function variants indicate TRPM3 as the cause of a spectrum of autosomal dominant neurodevelopmental disorders with frequent cerebellar involvement in humans.

Genetic finding of pathogenic CRMP1 variants in three unrelated individuals with neurodevelopmental disorder, supported by structural simulation, biochemical and proof-of-principle data highlights the key role of CRMP1 in the development and functioning of the nervous system in humans.

The multimodal linked independent component analysis promotes a more integrative understanding of transdiagnostic mechanisms of psychopathology.

lnc-Nr2f1, a long non-coding RNA focally deleted in autism patients, directly occupies and regulates neuronal genes.

Successful autism spectrum disorder gene discovery using forward genetics identifies KDM5A, which encodes a histone H3 lysine 4 demethylase, as a disease gene.

Severe neurodevelopmental disorder risk gene functions are retained into adulthood and they contribute to disease phenotypes, indicating that these patients may respond to treatments throughout life.

Chronic dysregulation of matrix-metalloproteinase 9, which is associated with some neurodevelopmental disorders, leads to local hyperconnectivity in the developing brain, resulting in altered sensory processing and increased seizure susceptibility.

Learning in children with autism spectrum disorder (ASD) was achieved by fundamentally different cognitive and neural mechanisms from typically developing children, and insistence on sameness, a core symptom of ASD, contributed to such atypical mechanisms of learning in affected children.

Spatiotemporal manipulations of insomniac reveal that this gene regulates the birth and development of sleep-regulatory neurons, enabling their proper function in adulthood.