ArticleNature neuroscience2019
Pathological priming causes developmental gene network heterochronicity in autistic subject-derived neurons.
Article in Nature neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
161 citing papers in PubMed, 1 synthesis or guideline pooled it, 313 citations in OpenAlex.
- Uncovering convergence and divergence between autism and schizophrenia using genomic tools and patients' neurons.Molecular psychiatry · 2025Pooled it
- Pathological Priming and Developmental Heterochrony as Organizing Concepts in Human iPSC Models of Autism Spectrum Disorder.Molecular neurobiology · 2026Review
- Circulating neuronal proteins are elevated in severe autism and associated with patient-specific neuronal dysfunction and behavioral deficits.Translational psychiatry · 2026Article
- An electrophysiological and proteomics roadmap for human induced glutamatergic neurons: fine-tuning of culture conditions for pathophysiological studies.Cell death discovery · 2026Article
- "SHANK3 deficiency alters early progenitor dynamics and reveals shared pathways with neurodegeneration".Molecular psychiatry · 2026Article
- MECP2 mutations rewire human ESC fate and bias cortical lineage commitment.Stem cell reports · 2026Article
- Functional impact of genetic background on variable expressivity in neurodevelopmental disorders.Nature communications · 2026Article
- CK2 inhibition suppresses glial inflammation in models of neuroinflammation and neurodegeneration.Nature communications · 2026Article
- A scalable human-zebrafish xenotransplantation model reveals gastrosome-mediated processing of dying neurons by human microglia.Communications biology · 2026Article
- Modulating alternative splicing ofScience translational medicine · 2026Article
- Article
- Pharmacological manipulation of nested oscillations in human iPSC-derived 2D neuronal networks.Neurobiology of disease · 2026Article
- Extracellular vesicles from stem cells rescue cellular phenotypes and behavioral deficits in SHANK3-associated ASD neuronal and mouse models.Cell death & disease · 2026Article
- Aberrant neural stem cell quiescence is the gateway to autism development linked to Arid1b.Molecular psychiatry · 2026Article
- Human cortical organoids recapitulate inter-individual variability in infant brain-growth trajectories.Cell stem cell · 2026Article
- A scoping review of stem cell models of leukodystrophies: advances in understanding pathophysiological mechanisms.NPJ genomic medicine · 2025Article
- A splice-switching antisense oligonucleotide approach for pediatric genetic epilepsies.bioRxiv : the preprint server for biology · 2025Article
- Analysis of neuronal activity impairment in iPSC-derived neurons from idiopathic autism patients.iScience · 2025Article
- Digestive Neurobiology in Autism: From Enteric and Central Nervous System Interactions to Shared Genetic Pathways.International journal of molecular sciences · 2025Review
- Functional Neurogenomics to Dissect Disease Mechanisms Across Models.Annual review of genomics and human genetics · 2025Review
101 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 5 countries.
Funding
Abstract
Autism spectrum disorder (ASD) is thought to emerge during early cortical development. However, the exact developmental stages and associated molecular networks that prime disease propensity are elusive. To profile early neurodevelopmental alterations in ASD with macrocephaly, we monitored subject-derived induced pluripotent stem cells (iPSCs) throughout the recapitulation of cortical development. Our analysis revealed ASD-associated changes in the maturational sequence of early neuron development, involving temporal dysregulation of specific gene networks and morphological growth acceleration. The observed changes tracked back to a pathologically primed stage in neural stem cells (NSCs), reflected by altered chromatin accessibility. Concerted over-representation of network factors in control NSCs was sufficient to trigger ASD-like features, and circumventing the NSC stage by direct conversion of ASD iPSCs into induced neurons abolished ASD-associated phenotypes. Our findings identify heterochronic dynamics of a gene network that, while established earlier in development, contributes to subsequent neurodevelopmental aberrations in ASD.
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Registered trials
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 OpenQuestion graph.