ArticleFrontiers in neuroscience2022
Asynchronous excitatory neuron development in an isogenic cortical spheroid model of Down syndrome.
Article in Frontiers in neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 16 citations in OpenAlex.
- A Researcher's guide to rodent models of Down syndrome: Recent insights and translational perspectives.STAR protocols · 2026Review
- Disrupted Vestibular Nuclei Neuron Development in a Chick Model for Congenital Vestibular Disorders.Developmental neurobiology · 2026Article
- Transcriptional and functional profiles of muscarinic receptor-expressing neurons in primate lateral prefrontal and anterior cingulate cortices.Communications biology · 2026Article
- Single-cell atlas of the developing Down syndrome brain cortex.Nature medicine · 2026Article
- A pipeline for cell migration analysis in live-cell imaging data from human iPSC-derived forebrain assembloids.Frontiers in cell and developmental biology · 2026Article
- Seeing clearly with CLARI-O: a window into cellular architecture, interactions, and morphology of organoid models.Frontiers in neuroscience · 2026Article
- A neurorecording toolkit for longitudinal assessments of transplanted human cortical organoidsbioRxiv : the preprint server for biology · 2025Article
- Disrupted Neurogenesis from Basal Intermediate Precursor Cells Alters the Postnatal Neocortex in the TcMAC21 Mouse Model of Down Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Longitudinal Proteomic Changes in HCT 116 Colon Cancer Spheroids During Growth.Journal of proteome research · 2025Article
- Reduction of inflammatory biomarkers underlies extracellular vesicle mediated functional recovery in an aged monkey model of cortical injury.Frontiers in aging neuroscience · 2025Article
- Brain volumes, cognitive, and adaptive skills in school-age children with Down syndrome.Journal of neurodevelopmental disorders · 2024Article
- Consequences of trisomy 21 for brain development in Down syndrome.Nature reviews. Neuroscience · 2024Review
- Transcriptional consequences of trisomy 21 on neural induction.Frontiers in cellular neuroscience · 2024Article
- Extracellular Vesicle Treatment Alleviates Neurodevelopmental and Neurodegenerative Pathology in Cortical Spheroid Model of Down Syndrome.International journal of molecular sciences · 2023Article
- From neurodevelopment to neurodegeneration: utilizing human stem cell models to gain insight into Down syndrome.Frontiers in genetics · 2023Review
- Shaking up the silence: consequences of HMGN1 antagonizing PRC2 in the Down syndrome brain.Epigenetics & chromatin · 2022Review
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Authors and funding
8 authors at 2 institutions in 1 country.
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Abstract
The intellectual disability (ID) in Down syndrome (DS) is thought to result from a variety of developmental deficits such as alterations in neural progenitor division, neurogenesis, gliogenesis, cortical architecture, and reduced cortical volume. However, the molecular processes underlying these neurodevelopmental changes are still elusive, preventing an understanding of the mechanistic basis of ID in DS. In this study, we used a pair of isogenic (trisomic and euploid) induced pluripotent stem cell (iPSC) lines to generate cortical spheroids (CS) that model the impact of trisomy 21 on brain development. Cortical spheroids contain neurons, astrocytes, and oligodendrocytes and they are widely used to approximate early neurodevelopment. Using single cell RNA sequencing (scRNA-seq), we uncovered cell type-specific transcriptomic changes in the trisomic CS. In particular, we found that excitatory neuron populations were most affected and that a specific population of cells with a transcriptomic profile resembling layer IV cortical neurons displayed the most profound divergence in developmental trajectory between trisomic and euploid genotypes. We also identified candidate genes potentially driving the developmental asynchrony between trisomic and euploid excitatory neurons. Direct comparison between the current isogenic CS scRNA-seq data and previously published datasets revealed several recurring differentially expressed genes between DS and control samples. Altogether, our study highlights the power and importance of cell type-specific analyses within a defined genetic background, coupled with broader examination of mixed samples, to comprehensively evaluate cellular phenotypes in the context of DS.
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