ArticleNature communications2025
Early developmental origins of cortical disorders modeled in human neural stem cells.
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 8 papers.
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Who cites it
8 citing papers in PubMed.
- Multiomics analysis identifies VPA-induced changes in neural progenitor cells, ventricular-like regions, and cellular microenvironment in dorsal forebrain organoids.Molecular psychiatry · 2026Article
- Article
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- Perinatal brain developmental transition revealed by transcriptomic and proteomic analyses of Bama miniature pigs.Nature communications · 2026Article
- NeMO Analytics: a compendium of transcriptomic data for the exploration of neocortical development.Nature neuroscience · 2026Article
- Establishing Area-Specific Brain Organoids Through Transcription Factor-Mediated Patterning.Biology · 2026Article
- Dominant and recessive ATOH1 variants cause distinct neurodevelopmental disorders with hearing loss.American journal of human genetics · 2026Article
- Progenitor diversity during formation of the mammalian neocortex.Frontiers in neuroscience · 2026Review
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16 authors.
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Abstract
The implications of the early phases of human telencephalic development, involving neural stem cells (NSCs), in the etiology of cortical disorders remain elusive. Here, we explore the expression dynamics of cortical and neuropsychiatric disorder-associated genes in datasets generated from human NSCs across telencephalic fate transitions in vitro and in vivo. We identify risk genes expressed in brain organizers and sequential gene regulatory networks throughout corticogenesis, revealing disease-specific critical phases when NSCs may be more vulnerable to gene dysfunction and converging signaling across multiple diseases. Further, we simulate the impact of risk transcription factor (TF) depletions on neural cell trajectories traversing human corticogenesis and observe a spatiotemporal-dependent effect for each perturbation. Finally, single-cell transcriptomics of autism-affected patient-derived NSCs in vitro reveals recurrent expression alteration of TFs orchestrating brain patterning and NSC lineage commitment. This work opens perspectives to explore human brain dysfunction at early phases of development.
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