ArticleNeuroscience letters2025
C1ql3 promotes cognitive flexibility behavior in mice.
Article in Neuroscience letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Brain-Wide Mapping and Synaptic Localization of C1QL3 Using a Novel Epitope-Tagged Knock-In Mouse.The Journal of comparative neurology · 2026Article
- Hsa-miR-25-3p Inhibition Sensitizes Patient-Derived Glioblastoma Cells to Temozolomide via β-catenin Downregulation.Cellular and molecular neurobiology · 2026Article
- Backbone resonance assignment of the pentraxin domain of the neuronal pentraxin receptor (NPTXR).Biomolecular NMR assignments · 2026Article
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Authors and funding
10 authors.
Funding
Abstract
Cognitive flexibility, the ability to adapt behavioral strategies based on changing circumstances, is deficient in patients with certain neuropsychiatric disorders, such as autism spectrum disorder and schizophrenia. Cognitive flexibility can be measured in humans and animal models using attentional set-shifting tasks, which require activity of the prefrontal cortex (PFC) and other key brain regions. We demonstrate that C1QL3, a protein involved in regulating excitatory synapse density in the PFC and other brain circuits, is important for attentional set-shifting, using a mouse model of C1ql3 disruption. Conditional deletion of C1ql3 from neurons specifically in the PFC of adult mice was not sufficient to impair attentional set-shifting behavior, highlighting the potential role of C1ql3 in promoting cognitive flexibility through expression in other key brain circuits and/or neurodevelopmental processes.
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Registered trials
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