ArticleCell2013
Spatial and temporal mapping of de novo mutations in schizophrenia to a fetal prefrontal cortical network.
Article in Cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 360 papers, 5 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
360 citing papers in PubMed, 5 syntheses or guidelines pooled it, 565 citations in OpenAlex.
- Mapping protein states and interactions across the tree of life with co-fractionation mass spectrometry.Nature communications · 2023Pooled it
- Multi-ancestry genome-wide association study of cannabis use disorder yields insight into disease biology and public health implications.Nature genetics · 2023Pooled it
- A Systematic Review of the Human Accelerated Regions in Schizophrenia and Related Disorders: Where the Evolutionary and Neurodevelopmental Hypotheses Converge.International journal of molecular sciences · 2023Pooled it
- Analysing an allelic series of rare missense variants of CACNA1I in a Swedish schizophrenia cohort.Brain : a journal of neurology · 2022Pooled it
- Genome-wide association study followed by trans-ancestry meta-analysis identify 17 new risk loci for schizophrenia.BMC medicine · 2021Pooled it
- Effect of Damaging Rare Mutations in Synapse-Related Gene Sets on Response to Short-term Antipsychotic Medication in Chinese Patients With Schizophrenia: A Randomized Clinical Trial.JAMA psychiatry · 2018Trial
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- Chromatin-associated intronic RNAs from long genes form introsomes that shape nuclear architecture in neuronal cells.bioRxiv : the preprint server for biology · 2026Article
- 3D genetic architecture of schizophrenia risk across three neuronal subtypes.Molecular psychiatry · 2026Article
- Mild SARS-CoV-2 maternal infection in mice induces transient offspring neurodevelopmental aberrance.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Recurrent and Non-Recurrent Copy Number Variants in Native Americans and a Cosmopolitan Sample in Relation to Alcohol Use Disorder and Other Psychiatric Diseases.Molecular neurobiology · 2026Article
- Loss of function of the chromatin remodeling geneProceedings of the National Academy of Sciences of the United States of America · 2026Article
- In vivo mapping of protein-protein interactions of schizophrenia risk factors generates an interconnected disease network.Schizophrenia (Heidelberg, Germany) · 2026Article
- Neuronal guidance signaling in neurodegenerative diseases: Key regulators that function at neuron-glia and neuroimmune interfaces.Neural regeneration research · 2026Article
- Functional implications of polygenic risk for schizophrenia in human neurons.Nature communications · 2026Article
- A Tousled-like kinase (TLK) homolog required for male germline stem cell homeostasis in the planarian Schmidtea mediterranea.Developmental biology · 2026Article
- A Retinoic Acid Autoregulatory Loop Governing Prefrontal-Motor Arealization.bioRxiv : the preprint server for biology · 2025Article
- Recurrent & non-recurrent copy number variants in Native Americans and a cosmopolitan sample in relation to Alcohol Use Disorder and other psychiatric diseases.Research square · 2025Article
300 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 6 institutions in 2 countries.
Funding
Abstract
Genes disrupted in schizophrenia may be revealed by de novo mutations in affected persons from otherwise healthy families. Furthermore, during normal brain development, genes are expressed in patterns specific to developmental stage and neuroanatomical structure. We identified de novo mutations in persons with schizophrenia and then mapped the responsible genes onto transcriptome profiles of normal human brain tissues from age 13 weeks gestation to adulthood. In the dorsolateral and ventrolateral prefrontal cortex during fetal development, genes harboring damaging de novo mutations in schizophrenia formed a network significantly enriched for transcriptional coexpression and protein interaction. The 50 genes in the network function in neuronal migration, synaptic transmission, signaling, transcriptional regulation, and transport. These results suggest that disruptions of fetal prefrontal cortical neurogenesis are critical to the pathophysiology of schizophrenia. These results also support the feasibility of integrating genomic and transcriptome analyses to map critical neurodevelopmental processes in time and space in the brain.
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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.