ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
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.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- δ-catenin controls layer-specific transcriptional maturation of astrocytes via Zbtb20.bioRxiv : the preprint server for biology · 2026Article
- δ-catenin haploinsufficiency is sufficient to alter behaviors and glutamatergic synapses in mice.Neuroscience · 2026Article
- Early Life PBDE Flame Retardant Exposures Cause Neurobehavioral Alterations in Fish That Persist into Adulthood and Vary by Sex and Route of Exposure.Environmental science & technology · 2025Article
- Comparative analysis of two newly established Cre rat lines, NeuN-Cre and Thy1-Cre, for neurological research.Animal models and experimental medicine · 2025Article
- 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.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Roles and regulation of δ-catenin in tumorigenesis and neuronal diseases.Frontiers in cell and developmental biology · 2025Review
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Authors and funding
12 authors.
Funding
Abstract
The Cri du Chat Syndrome (CdCS), a devastating genetic disorder caused by a deletion on chromosome 5p, faces challenges in finding effective treatments and accurate animal models. Using CRISPR-Cas9, 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-seq analyses provide new insights into CdCS pathogenesis, revealing inflammatory and immune processes. Importantly, it is demonstrated that early gene replacement therapy with AAV-Ctnnd2 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.
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