ArticleTranslational psychiatry2020
Comprehensive analysis of a novel mouse model of the 22q11.2 deletion syndrome: a model with the most common 3.0-Mb deletion at the human 22q11.2 locus.
Article in Translational psychiatry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 54 citations in OpenAlex.
- Animal Models for Drug Discovery in Schizophrenia: A Critical View from a Clinical Perspective.Pharmaceutical medicine · 2026Review
- Divergent transcriptomic pathways underlie sex-biased cognitive rescue by developmental GSK3B inhibition in a mouse model of 22q11.2 deletion syndrome.Translational psychiatry · 2026Article
- A microbiome quantitative trait locus in SLC39A8 modulates disease severity in synucleinopathy-induced models of Parkinson's disease.Human molecular genetics · 2026Article
- Neonatal social communication and single genes predict the variability of post-pubertal social behavior in a mouse model of paternal 15q11-13 duplication.Research square · 2026Article
- Suppressive Genetic Interactions Between Haploinsufficient Mitochondrial Genes Encoded in the 22q11.2 Microdeletion Locus Define Brain and Cardiac Phenotypes.bioRxiv : the preprint server for biology · 2026Article
- Minoxidil restores thymic growth in 22q11.2 deletion syndrome by limiting Sox9Journal of human immunity · 2025Article
- Article
- Unraveling the enigma of mental disorders: a genetics-first approach and the role of mouse models based on rare disease-susceptible genome variants.Nagoya journal of medical science · 2025Review
- Highly demarcated structural alterations in the brain and impaired social incentive learning in Tbx1 heterozygous mice.Molecular psychiatry · 2025Article
- The acoustic startle response in 22q11 deletion syndrome: from animal models to humans.Frontiers in neuroscience · 2025Review
- Tbx1 haploinsufficiency leads to local skull deformity, paraflocculus and flocculus dysplasia, and motor-learning deficit in 22q11.2 deletion syndrome.Nature communications · 2024Article
- Progress towards understanding risk factor mechanisms in the development of autism spectrum disorders.Biochemical Society transactions · 2024Review
- Hyperactive mTORC1 in striatum dysregulates dopamine receptor expression and odor preference behavior.Frontiers in neuroscience · 2024Article
- Review: Genes Involved in Mitochondrial Physiology Within 22q11.2 Deleted Region and Their Relevance to Schizophrenia.Schizophrenia bulletin · 2023Article
- Sleep in 22q11.2 Deletion Syndrome: Current Findings, Challenges, and Future Directions.Current psychiatry reports · 2023Review
- Ileal Dysbiosis Is Associated with Increased Acoustic Startle in the 22q11.2 Microdeletion Mouse Model of Schizophrenia.Nutrients · 2023Article
- Structural alterations in the amygdala and impaired social incentive learning in a mouse model of a genetic variant associated with neurodevelopmental disorders.Research square · 2023Article
- Shedding light on latent pathogenesis and pathophysiology of mental disorders: The potential of iPS cell technology.Psychiatry and clinical neurosciences · 2023Review
- The molecular pathology of schizophrenia: an overview of existing knowledge and new directions for future research.Molecular psychiatry · 2023Review
- Article
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Authors and funding
19 authors at 3 institutions in 1 country.
Funding
Abstract
The 22q11.2 deletion syndrome (22q11.2DS) is associated with an increased risk for psychiatric disorders. Although most of the 22q11.2DS patients have a 3.0-Mb deletion, existing mouse models only mimic a minor mutation of 22q11.2DS, a 1.5-Mb deletion. The role of the genes existing outside the 1.5-Mb deletion in psychiatric symptoms of 22q11.2DS is unclear. In this study, we generated a mouse model that reproduced the 3.0-Mb deletion of the 22q11.2DS (Del(3.0 Mb)/ +) using the CRISPR/Cas9 system. Ethological and physiological phenotypes of adult male mutants were comprehensively evaluated by visual-evoked potentials, circadian behavioral rhythm, and a series of behavioral tests, such as measurement of locomotor activity, prepulse inhibition, fear-conditioning memory, and visual discrimination learning. As a result, Del(3.0 Mb)/ + mice showed reduction of auditory prepulse inhibition and attenuated cue-dependent fear memory, which is consistent with the phenotypes of existing 22q11.2DS models. In addition, Del(3.0 Mb)/ + mice displayed an impaired early visual processing that is commonly seen in patients with schizophrenia. Meanwhile, unlike the existing models, Del(3.0 Mb)/ + mice exhibited hypoactivity over several behavioral tests, possibly reflecting the fatigability of 22q11.2DS patients. Lastly, Del(3.0 Mb)/ + mice displayed a faster adaptation to experimental jet lag as compared with wild-type mice. Our results support the validity of Del(3.0 Mb)/ + mice as a schizophrenia animal model and suggest that our mouse model is a useful resource to understand pathogenic mechanisms of schizophrenia and other psychiatric disorders associated with 22q11.2DS.
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