Circuit mechanism underlying fragmented sleep and memory deficits in 16p11.2 deletion mouse model of autism.

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Researchers studying mice with the 16p11.2 deletion found that overactive brain cells called locus coeruleus noradrenergic (LC-NE) neurons cause fragmented sleep and memory problems, and that calming these neurons—using a drug called clonidine or light-based techniques—can restore more normal sleep and improve memory, offering a potential treatment target for families dealing with sleep and cognitive challenges.