Autism is a neurodevelopmental disorder that impairs development of speech and social interactions, and this disorder affects more than 20 million people worldwide. It is believed that autism disrupts the processing of information in the brain by changing synaptic connectivity, but the exact mechanism of impairment is not yet known. Autism must therefore be diagnosed behaviorally as children progress through developmental milestones; this limits the developmental stage at which treatments and interventions can be administered. A key question in autism research, therefore, is whether aspects of the pathology can be reversed later in development and adulthood.
A recent study directly addressed this issue by manipulating levels of the Shank3 gene, which encodes a scaffolding protein of excitatory synapses that is involved in ∼1% of autism spectrum disorder cases (Nature 530, 481–484; 2016). Using a novel transgenic mouse model, the research group showed that rescuing Shank3 expression in adulthood led to a reversal of some—but not all—autistic phenotypes, including social interactions and repetitive grooming behaviors. Their data demonstrate that treatments for autism, even when applied later in development, might be able to reverse certain symptoms, and this study further highlights the continued plasticity of the brain into adulthood. DMG
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