ArticleMolecular psychiatry2014
Neuroanatomical phenotypes in a mouse model of the 22q11.2 microdeletion.
Article in Molecular psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 72 citations in OpenAlex.
- Neuronal ensembles in cortical function and disease.Physiological reviews · 2026Review
- An ace in the hole? Opportunities and limits of using mice to understand schizophrenia neurobiology.Molecular psychiatry · 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
- Running in the FAMILY: understanding and predicting the intergenerational transmission of mental illness.European child & adolescent psychiatry · 2024Article
- Mitochondrial proteins encoded by the 22q11.2 neurodevelopmental locus regulate neural stem and progenitor cell proliferation.Molecular psychiatry · 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
- Article
- Mitochondrial genes in the 22q11.2 deleted region regulate neural stem and progenitor cell proliferation.bioRxiv : the preprint server for biology · 2023Article
- A Comprehensive Analysis of Cerebellar Volumes in the 22q11.2 Deletion Syndrome.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2023Article
- 17q12 deletion syndrome mouse model shows defects in craniofacial, brain and kidney development, and glucose homeostasis.Disease models & mechanisms · 2022Article
- The 22q11.2 region regulates presynaptic gene-products linked to schizophrenia.Nature communications · 2022Article
- Advantages and Limitations of Animal Schizophrenia Models.International journal of molecular sciences · 2022Review
- Translational Magnetic Resonance Imaging in Autism Spectrum Disorder From the Mouse Model to Human.Frontiers in neuroscience · 2022Review
- Cognitive Deficit in Schizophrenia: From Etiology to Novel Treatments.International journal of molecular sciences · 2021Review
- Neuroanatomy and behavior in mice with a haploinsufficiency of AT-rich interactive domain 1B (ARID1B) throughout development.Molecular autism · 2021Article
- A Selective Review of the Excitatory-Inhibitory Imbalance in Schizophrenia: Underlying Biology, Genetics, Microcircuits, and Symptoms.Frontiers in cell and developmental biology · 2021Review
- Large-scale mapping of cortical alterations in 22q11.2 deletion syndrome: Convergence with idiopathic psychosis and effects of deletion size.Molecular psychiatry · 2020Article
- Schizophrenia-related microdeletion causes defective ciliary motility and brain ventricle enlargement via microRNA-dependent mechanisms in mice.Nature communications · 2020Article
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Authors and funding
10 authors at 5 institutions in 3 countries.
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Abstract
Recurrent deletions at the 22q11.2 locus have been established as a strong genetic risk factor for the development of schizophrenia and cognitive dysfunction. Individuals with 22q11.2 deletions have a range of well-defined volumetric abnormalities in a number of critical brain structures. A mouse model of the 22q11.2 deletion (Df(16)A(+/-)) has previously been utilized to characterize disease-associated abnormalities on synaptic, cellular, neurocircuitry, and behavioral levels. We performed a high-resolution MRI analysis of mutant mice compared with wild-type littermates. Our analysis revealed a striking similarity in the specific volumetric changes of Df(16)A(+/-) mice compared with human 22q11.2 deletion carriers, including in cortico-cerebellar, cortico-striatal and cortico-limbic circuits. In addition, higher resolution magnetic resonance imaging compared with neuroimaging in human subjects allowed the detection of previously unknown subtle local differences. The cerebellar findings in Df(16)A(+/-) mice are particularly instructive as they are localized to specific areas within both the deep cerebellar nuclei and the cerebellar cortex. Our study indicates that the Df(16)A(+/-)mouse model recapitulates most of the hallmark neuroanatomical changes observed in 22q11.2 deletion carriers. Our findings will help guide the design and interpretation of additional complementary studies and thereby advance our understanding of the abnormal brain development underlying the emergence of 22q11.2 deletion-associated psychiatric and cognitive symptoms.
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