ArticleStem cell reports2022
Altered patterning of trisomy 21 interneuron progenitors.
Article in Stem cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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.
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Who cites it
24 citing papers in PubMed, 29 citations in OpenAlex.
- Disruption of hippocampal upstream regulators of mTOR and insulin pathways in Down syndrome with Alzheimer's disease neuropathology: Preliminary observations.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- A Researcher's guide to rodent models of Down syndrome: Recent insights and translational perspectives.STAR protocols · 2026Review
- Abnormal neuronal and synaptic morphology in Down syndrome brains reproduces in human isogenic cellular models.Cell death & disease · 2026Article
- Aberrant chromatin remodeling influences human neural cell fate change in Trisomy 21.bioRxiv : the preprint server for biology · 2026Article
- Leucettinib-21 decreases dosage effects of DYRK1A in human trisomy 21 induced pluripotent stem cell-derived neural cells.Disease models & mechanisms · 2026Article
- Single-cell atlas of the developing Down syndrome brain cortex.Nature medicine · 2026Article
- Leucettinib-21 decreases dosage effects of DYRK1A in human trisomy 21 iPSC-derived neural cells.bioRxiv : the preprint server for biology · 2026Article
- Development of Molecular Neuropathology in Down Syndrome across the Lifespan.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Review
- Vertebrate and Invertebrate Animal Models for the Study of Down Syndrome.International journal of molecular sciences · 2025Review
- The Hallmarks of Aneuploidy in Cancer and Congenital Syndromes.Annual review of genomics and human genetics · 2025Review
- Analysis of genotype effects and inter-individual variability in iPSC-derived trisomy 21 neural progenitor cells.Human molecular genetics · 2025Article
- The restoration of REST inhibits reactivity of Down syndrome iPSC-derived astrocytes.Frontiers in molecular neuroscience · 2025Article
- Consequences of trisomy 21 for brain development in Down syndrome.Nature reviews. Neuroscience · 2024Review
- A scalable, high-throughput neural development platform identifies shared impact of ASD genes on cell fate and differentiation.bioRxiv : the preprint server for biology · 2024Article
- A dynamic in vitro model of Down syndrome neurogenesis with trisomy 21 gene dosage correction.Science advances · 2024Article
- Transcriptional consequences of trisomy 21 on neural induction.Frontiers in cellular neuroscience · 2024Article
- Article
- Cognitive impairments in a Down syndrome model with abnormal hippocampal and prefrontal dynamics and cytoarchitecture.iScience · 2023Article
- Extracellular Vesicle Treatment Alleviates Neurodevelopmental and Neurodegenerative Pathology in Cortical Spheroid Model of Down Syndrome.International journal of molecular sciences · 2023Article
- Review
Corrections and comments
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Authors and funding
19 authors at 1 institution in 1 country.
Funding
Abstract
Individuals with Down syndrome (DS; Ts21), the most common genetic cause of intellectual disability, have smaller brains that reflect fewer neurons at pre- and post-natal stages, implicating impaired neurogenesis during development. Our stereological analysis of adult DS cortex indicates a reduction of calretinin-expressing interneurons. Using Ts21 human induced pluripotent stem cells (iPSCs) and isogenic controls, we find that Ts21 progenitors generate fewer COUP-TFII+ progenitors with reduced proliferation. Single-cell RNA sequencing of Ts21 progenitors confirms the altered specification of progenitor subpopulations and identifies reduced WNT signaling. Activation of WNT signaling partially restores the COUP-TFII+ progenitor population in Ts21, suggesting that altered WNT signaling contributes to the defective development of cortical interneurons in DS.
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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.