ArticleMolecular psychiatry2021
Transcriptomic networks implicate neuronal energetic abnormalities in three mouse models harboring autism and schizophrenia-associated mutations.
Article in Molecular psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- Identification of hub genes involved in early-onset schizophrenia: from genetic susceptibility to predicted regulated gene expression.Molecular psychiatry · 2026Article
- Developmentally dynamic, non-convergent transcriptomic profiles in CNV models for schizophrenia risk.Molecular psychiatry · 2026Article
- Review
- Identification of Hub Genes Involved in Early-onset Schizophrenia: From Genetic Susceptibility to Predicted Regulated Gene Expression.Research square · 2025Article
- A review on the relationship between the distal 1q21.1 microdeletion and schizophrenia.Frontiers in genetics · 2025Review
- Schizophrenia genomics: genetic complexity and functional insights.Nature reviews. Neuroscience · 2024Review
- Altered projection-specific synaptic remodeling and its modification by oxytocin in an idiopathic autism marmoset model.Communications biology · 2024Article
- Cross-species analysis identifies mitochondrial dysregulation as a functional consequence of the schizophrenia-associated 3q29 deletion.Science advances · 2023Article
- Autistic spectrum disorder (ASD) - Gene, molecular and pathway signatures linking systemic inflammation, mitochondrial dysfunction, transsynaptic signalling, and neurodevelopment.Brain, behavior, & immunity - health · 2023Article
- Impaired OTUD7A-dependent Ankyrin regulation mediates neuronal dysfunction in mouse and human models of the 15q13.3 microdeletion syndrome.Molecular psychiatry · 2023Article
- Altered gene expression profiles impair the nervous system development in individuals with 15q13.3 microdeletion.Scientific reports · 2022Article
- Deepening the understanding of CNVs on chromosome 15q11-13 by using hiPSCs: An overview.Frontiers in cell and developmental biology · 2022Review
- The Brain Is Adaptive Not Triune: How the Brain Responds to Threat, Challenge, and Change.Frontiers in psychiatry · 2022Review
- Genetic contributions to autism spectrum disorder.Psychological medicine · 2021Review
- Convergent and distributed effects of the 3q29 deletion on the human neural transcriptome.Translational psychiatry · 2021Article
- Prioritizing Genetic Contributors to Cortical Alterations in 22q11.2 Deletion Syndrome Using Imaging Transcriptomics.Cerebral cortex (New York, N.Y. : 1991) · 2021Article
- Copy number variation and neuropsychiatric illness.Current opinion in genetics & development · 2021Review
- Dissecting Molecular Genetic Mechanisms of 1q21.1 CNV in Neuropsychiatric Disorders.International journal of molecular sciences · 2021Review
- Advances in autism research, 2021: continuing to decipher the secrets of autism.Molecular psychiatry · 2021Article
- Network Effects of the 15q13.3 Microdeletion on the Transcriptome and Epigenome in Human-Induced Neurons.Biological psychiatry · 2021Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
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Abstract
Genetic risk for psychiatric illness is complex, so identification of shared molecular pathways where distinct forms of genetic risk might coincide is of substantial interest. A growing body of genetic and genomic studies suggest that such shared molecular pathways exist across disorders with different clinical presentations, such as schizophrenia and autism spectrum disorder (ASD). But how this relates to specific genetic risk factors is unknown. Further, whether some of the molecular changes identified in brain relate to potentially confounding antemortem or postmortem factors are difficult to prove. We analyzed the transcriptome from the cortex and hippocampus of three mouse lines modeling human copy number variants (CNVs) associated with schizophrenia and ASD: Df(h15q13)/+, Df(h22q11)/+, and Df(h1q21)/+ which carry the 15q13.3 deletion, 22q11.2 deletion, and 1q21.1 deletion, respectively. Although we found very little overlap of differential expression at the level of individual genes, gene network analysis identified two cortical and two hippocampal modules of co-expressed genes that were dysregulated across all three mouse models. One cortical module was associated with neuronal energetics and firing rate, and overlapped with changes identified in postmortem human brain from SCZ and ASD patients. These data highlight aspects of convergent gene expression in mouse models harboring major risk alleles, and strengthen the connection between changes in neuronal energetics and neuropsychiatric disorders in humans.
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