ArticleMolecular psychiatry2019
Reversal of proliferation deficits caused by chromosome 16p13.11 microduplication through targeting NFκB signaling: an integrated study of patient-derived neuronal precursor cells, cerebral organoids and in vivo brain imaging.
Article in Molecular psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mapping the Cerebral Organoid Landscape: A Systematic Review of Preclinical 3D Models in Neuroscience.Advanced healthcare materials · 2026Pooled it
- Using Brain Organoids to Explore Human Neurobiology.Cellular and molecular neurobiology · 2026Review
- ASD mutations in the ciliary gene CEP41 impact development of projection neurons and interneurons in a human cortical organoid model.Molecular psychiatry · 2026Article
- The EH-binding protein EHBP1 operates in a ciliary functional module affected by INPP5E dysfunction.Journal of cell science · 2026Article
- Rare Copy Number Variants Reveal Critical Cell Types and Periods of Brain Development in Neurodevelopmental Disorders.Biological psychiatry global open science · 2025Article
- Perturbed cell fate decision by schizophrenia-associated AS3MTScience advances · 2025Article
- Altered neuroepithelial morphogenesis and migration defects in iPSC-derived cerebral organoids and 2D neural stem cells in familial bipolar disorder.Oxford open neuroscience · 2024Article
- Article
- Abnormalities in the migration of neural precursor cells in familial bipolar disorder.Disease models & mechanisms · 2022Article
- The ciliary gene INPP5E confers dorsal telencephalic identity to human cortical organoids by negatively regulating Sonic hedgehog signaling.Cell reports · 2022Article
- Region Specific Brain Organoids to Study Neurodevelopmental Disorders.International journal of stem cells · 2022Review
- 16p13.11 deletion variants associated with neuropsychiatric disorders cause morphological and synaptic changes in induced pluripotent stem cell-derived neurons.Frontiers in psychiatry · 2022Article
- What Makes Organoids Good Models of Human Neurogenesis?Frontiers in neuroscience · 2022Article
- Next-generation gene panel testing in adolescents and adults in a medical neuropsychiatric genetics clinic.Neurogenetics · 2021Article
- Cellular Models in Schizophrenia Research.International journal of molecular sciences · 2021Review
- Review
- DSCAM/PAK1 pathway suppression reverses neurogenesis deficits in iPSC-derived cerebral organoids from patients with Down syndrome.The Journal of clinical investigation · 2021Article
- Overexpression of CD47 is associated with brain overgrowth and 16p11.2 deletion syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Modeling neurological disorders using brain organoids.Seminars in cell & developmental biology · 2021Review
- The Multifaceted Roles of Primary Cilia in the Development of the Cerebral Cortex.Frontiers in cell and developmental biology · 2021Review
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22 authors.
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Abstract
The molecular basis of how chromosome 16p13.11 microduplication leads to major psychiatric disorders is unknown. Here we have undertaken brain imaging of patients carrying microduplications in chromosome 16p13.11 and unaffected family controls, in parallel with iPS cell-derived cerebral organoid studies of the same patients. Patient MRI revealed reduced cortical volume, and corresponding iPSC studies showed neural precursor cell (NPC) proliferation abnormalities and reduced organoid size, with the NPCs therein displaying altered planes of cell division. Transcriptomic analyses of NPCs uncovered a deficit in the NFκB p65 pathway, confirmed by proteomics. Moreover, both pharmacological and genetic correction of this deficit rescued the proliferation abnormality. Thus, chromosome 16p13.11 microduplication disturbs the normal programme of NPC proliferation to reduce cortical thickness due to a correctable deficit in the NFκB signalling pathway. This is the first study demonstrating a biologically relevant, potentially ameliorable, signalling pathway underlying chromosome 16p13.11 microduplication syndrome in patient-derived neuronal precursor cells.
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