Contribution of mGluR5 to pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion.

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Researchers studying mice with the same 16p11.2 deletion found that a brain receptor called mGluR5 contributes to memory problems, and that a medication targeting this receptor was able to reverse those cognitive deficits, offering a potential treatment direction for families affected by 16p11.2 deletion.