ArticleTranslational psychiatry2019
Cognitive impairment and autistic-like behaviour in SAPAP4-deficient mice.
Article in Translational psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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
12 citing papers in PubMed, 19 citations in OpenAlex.
- Psilocybin restores social novelty investigation in male SAPAP3 knockout mice and engages prefrontal-hippocampal circuitry.Molecular psychiatry · 2026Article
- Modeling Synaptic Maturation From Growth Cone to Synapse in Human Organoids.Journal of neurochemistry · 2026Article
- Involvement of membrane palmitoylated protein 6 (MPP6) in synapses of mouse cerebrum.Histochemistry and cell biology · 2025Article
- Quantitative proteomics of dorsolateral prefrontal cortex reveals an early pattern of synaptic dysmaturation in children with idiopathic autism.Cerebral cortex (New York, N.Y. : 1991) · 2024Article
- Review
- Novel role of the synaptic scaffold protein Dlgap4 in ventricular surface integrity and neuronal migration during cortical development.Nature communications · 2022Article
- Genotype-dependent epigenetic regulation of DLGAP2 in alcohol use and dependence.Molecular psychiatry · 2021Article
- Declining Levels of Specialized Synaptic Surface Proteins in nNOS-Expressing Interneurons in Mice Treated Prenatally with Valproic Acid.Neurochemical research · 2021Article
- A spatially resolved brain region- and cell type-specific isoform atlas of the postnatal mouse brain.Nature communications · 2021Article
- Molecular architecture of postsynaptic Interactomes.Cellular signalling · 2020Review
- Article
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Corrections and comments
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Authors and funding
24 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In humans, genetic variants of DLGAP1-4 have been linked with neuropsychiatric conditions, including autism spectrum disorder (ASD). While these findings implicate the encoded postsynaptic proteins, SAPAP1-4, in the etiology of neuropsychiatric conditions, underlying neurobiological mechanisms are unknown. To assess the contribution of SAPAP4 to these disorders, we characterized SAPAP4-deficient mice. Our study reveals that the loss of SAPAP4 triggers profound behavioural abnormalities, including cognitive deficits combined with impaired vocal communication and social interaction, phenotypes reminiscent of ASD in humans. These behavioural alterations of SAPAP4-deficient mice are associated with dramatic changes in synapse morphology, function and plasticity, indicating that SAPAP4 is critical for the development of functional neuronal networks and that mutations in the corresponding human gene, DLGAP4, may cause deficits in social and cognitive functioning relevant to ASD-like neurodevelopmental disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.