Autism spectrum disorders (ASD) represent neurodevelopmental and neuropsychiatric disorders characterized by social deficits and repetitive behaviors. ASD also accompanies many comorbidities, including intellectual disability, anxiety, ADHD-like hyperactivity, sensory abnormalities, and epilepsy. ASD affects ~1/36 people (2.8%) around the world, which is increasing at the rate of nearly two-fold every 10 years.
However, the underlying mechanisms are unclear, and effective treatments are unavailable. In particular, there is no widely accepted hypothesis for key mechanisms underlying ASD, which could be used to develop mechanism-based therapies. This is why many laboratories including ours are trying to identify key pathological mechanisms. Our lab is interested in testing if ASD is caused by synaptic dysfunctions such as impaired excitatory transmission involving NMDA receptors and the imbalance between excitatory and inhibitory synapses and neurons.
We are now focusing on characterizing multiple lines of mice carrying ASD-risk gene mutations and identifying key pathological mechanisms operating in different brain regions, cell types, and developmental stages. To this end, we try to combine approaches at molecular, synaptic, neuronal, circuit, and behavioral levels. In addition, our lab is interested in eventually determining if these mechanistic deviations observed in the mouse neural system are also observed in human neurons using stem cell approaches.
