ArticleNature communications2025
Aberrant pace of cortical neuron development in brain organoids from patients with 22q11.2 deletion syndrome-associated schizophrenia.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Tutorial: interrogating biology using organoid technologies.Nature protocols · 2026Review
- An antioxidant therapy elicits distinct transcriptome responses in 22q11-deleted upper layer cortical projection neurons.Disease models & mechanisms · 2026Article
- Gene dosage effects of 22q11.2 copy number variants on in-vivo measures of white matter axonal density and dispersion.Molecular psychiatry · 2026Article
- Convergent effects of neurodevelopmental disorder-associated variants at mitochondria.bioRxiv : the preprint server for biology · 2026Article
- Distinct cellular and transcriptional mechanisms mediate an antioxidant therapeutic response in 22q11-deleted upper layer cortical projection neurons.bioRxiv : the preprint server for biology · 2025Article
- The Etiological Role of Impaired Neurogenesis in Schizophrenia: Interactions with Inflammatory, Microbiome and Hormonal Signaling.International journal of molecular sciences · 2025Review
- Article
- CalciumZero: a toolbox for fluorescence calcium imaging on iPSC derived brain organoids.Brain informatics · 2025Article
- Regulation of the microprocessor by post-translational modifications.Frontiers in cell and developmental biology · 2025Review
- Thalamocortical organoids enable in vitro modeling of 22q11.2 microdeletion associated with neuropsychiatric disorders.Cell stem cell · 2024Article
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Authors and funding
14 authors.
Funding
Abstract
Children and adults with 22q11.2 deletion syndrome (22q11.2DS) experience cognitive and emotional challenges and face a markedly increased risk for schizophrenia (SCZ), yet how this deletion alters early human brain development remains unclear. Using cerebral cortex organoids derived from individuals with 22q11.2DS and SCZ, we identify cell-type-specific developmental abnormalities. Single-cell RNA sequencing and experimental validation reveal delayed cortical neuron maturation, with increased neural progenitor proliferation and a reduced proportion of more mature neurons. We observe disrupted molecular programs linked to neuronal maturation, sparser neurites, and blunted glutamate-induced Ca²⁺ responses. The aberrant transcriptional profile is enriched for neuropsychiatric risk genes. MicroRNA profiling suggests that DGCR8 haploinsufficiency contributes to these effects via dysregulation of genes that control the pace of maturation. Protein-protein interaction network analysis highlights complementary roles for additional deleted genes. Our study reveals consistent developmental and molecular defects caused by 22q11.2 deletions, offering insights into disease mechanisms and therapeutic strategies.
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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 Socratic graph.