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We systematically integrated scRNA\u2010seq data from 11 diverse genetic and environmental mouse (\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>Mus musculus<\/jats:italic>\n                    <\/jats:styled-content>\n                    ) models, encompassing &gt;\u2009300,000 cells across multiple brain regions and developmental stages. Using advanced computational harmonization (RPCA), we identified robust convergent transcriptomic signatures that transcend model\u2010specific variability. Our findings reveal widespread alterations in neuronal communication pathways, specifically increased excitatory\u2010inhibitory signaling involving PTN, SLIT, and PTPR pathways. Furthermore, cell\u2013cell communication analysis via NicheNet prioritized ligand\u2010receptor pairs associated with altered circuit excitability, offering a predictive blueprint of dysregulated intercellular crosstalk. Crucially, we identified significant glial involvement characterized by astrocyte function inhibition, marked by\n                    <jats:italic>Aqp4<\/jats:italic>\n                    and\n                    <jats:italic>Kcnj10<\/jats:italic>\n                    downregulation related to impaired water\/potassium homeostasis and mature oligodendrocyte metabolic dysregulation through\n                    <jats:italic>Olig<\/jats:italic>\n                    family upregulation and enhanced oxidative phosphorylation. Differentially expressed genes (DEGs) significantly overlapped with SFARI\u2010listed high\u2010confidence risk genes, particularly within excitatory neuronal subtypes. Comparison with human postmortem single\u2010nucleus data from the prefrontal and parietal cortices demonstrated conserved signatures related to impaired synaptic protein synthesis (GRIN2B, CAMK2A) and oligodendrocyte\u2010mediated neurodevelopmental deficits (NRXN, DLGAP). This study confirms that E\/I imbalance and glial dysfunction are universal cellular pathologies in ASD, providing a robust, large\u2010scale reference for identifying novel therapeutic targets with single\u2010cell resolution.\n                  <\/jats:p>","DOI":"10.1002\/glia.70225","type":"journal-article","created":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T15:56:03Z","timestamp":1792598163000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Single\u2010Cell Integration of Mouse Models of Autism Reveals Conserved Transcriptomic Signatures of Excitatory\u2010Inhibitory Imbalance and Glial Dysfunction"],"prefix":"10.1002","volume":"74","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4336-1709","authenticated-orcid":false,"given":"Jo\u00e3o V.","family":"Nani","sequence":"first","affiliation":[{"name":"Department of Biophysics, Escola Paulista de Medicina (EPM) Universidade Federal de S\u00e3o Paulo 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