The gut metabolite indole-3-propionic acid activates ERK1 to restore social function and hippocampal inhibitory synaptic transmission in a 16p11.2 microdeletion mouse model.

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Researchers discovered that a natural gut bacteria byproduct called indole-3-propionic acid (IPA) is reduced in mice with the 16p11.2 deletion, and that giving IPA as an oral supplement improved social behavior and memory by restoring brain signaling—offering a potentially promising treatment direction for families affected by 16p11.2 deletion syndrome.