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Adv."],"published-print":{"date-parts":[[2026,5,8]]},"abstract":"<jats:p>\n                    Mutations in\n                    <jats:italic toggle=\"yes\">SHANK3<\/jats:italic>\n                    are a leading monogenic cause of autism spectrum disorder (ASD), often associated with profound sensory abnormalities. However, the impact of\n                    <jats:italic toggle=\"yes\">SHANK3<\/jats:italic>\n                    deficiency on olfactory processing and the underlying neural mechanisms remains unclear. Here, we identify a cross-species disruption of olfactory valence perception in individuals with\n                    <jats:italic toggle=\"yes\">SHANK3<\/jats:italic>\n                    mutations and in\n                    <jats:italic toggle=\"yes\">Shank3<\/jats:italic>\n                    mutant mice. Patients carrying\n                    <jats:italic toggle=\"yes\">SHANK3<\/jats:italic>\n                    mutations exhibited impaired valence-oriented sniffing and electroencephalography (EEG) responses, whereas\n                    <jats:italic toggle=\"yes\">Shank3B<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice displayed blunted behavioral responses to both attractive and aversive odors. In mice, these behavioral deficits were associated with attenuated odor-evoked calcium signals and reduced excitatory synaptic transmission in the cortical amygdala (CoA), a key node for olfactory valence processing. Acute CoA-specific Shank3 deletion recapitulated these deficits, whereas targeted restoration of CoA Shank3 expression rescued odor-induced appetitive and aversive behaviors. Our findings reveal a conserved function for\n                    <jats:italic toggle=\"yes\">SHANK3<\/jats:italic>\n                    in encoding olfactory valence and identify CoA dysfunction as a circuit mechanism in mice.\n                  <\/jats:p>","DOI":"10.1126\/sciadv.aea3775","type":"journal-article","created":{"date-parts":[[2026,5,6]],"date-time":"2026-05-06T17:59:26Z","timestamp":1778090366000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":2,"title":["<i>SHANK3<\/i>\n                    mutations disrupt olfactory valence coding across species, with cortical amygdala mechanisms identified in mice"],"prefix":"10.1126","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0009-0001-2183-6582","authenticated-orcid":true,"given":"Yu","family":"Hu","sequence":"first","affiliation":[{"name":"Research Center for Primate Neuromodulation and Neuroimaging, Institute of Biomedical and Health Engineering, Shenzhen 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