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Using CRISPR\u2010Cas9, a novel CdCS rat model with a 2q22 deletion is developed, mirroring a common genetic alteration in CdCS patients. This model exhibits pronounced deficits in social behavior, cognition, and anxiety, accompanied by neuronal abnormalities and immune dysregulation in key brain regions such as the hippocampus and medial prefrontal cortex (mPFC). The immunostaining and RNA\u2010seq analyses provide new insights into CdCS pathogenesis, revealing inflammatory and immune processes. Importantly, it is demonstrated that early gene replacement therapy with AAV\u2010\n                    <jats:italic>Ctnnd2<\/jats:italic>\n                    alleviates cognitive impairments in CdCS rats, highlighting the potential for early intervention. However, the effectiveness of this therapy is confined to the early developmental stages and does not fully restore all CdCS symptoms. The findings deepen the understanding of CdCS pathogenesis and suggest promising therapeutic directions.\n                  <\/jats:p>","DOI":"10.1002\/advs.202415224","type":"journal-article","created":{"date-parts":[[2025,2,18]],"date-time":"2025-02-18T14:59:21Z","timestamp":1739890761000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Behavioral Abnormalities, Cognitive Impairments, Synaptic Deficits, and Gene Replacement Therapy in a CRISPR Engineered Rat Model of 5p15.2 Deletion Associated With Cri du Chat Syndrome"],"prefix":"10.1002","volume":"12","author":[{"given":"Jingjing","family":"Shen","sequence":"first","affiliation":[{"name":"Institute of Neuroscience School of Basic Medicine Chongqing Medical University  Chongqing 400016 China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yan","family":"Wang","sequence":"additional","affiliation":[{"name":"Institute of Neuroscience School of 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