ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
Role of founder cell deficit and delayed neuronogenesis in microencephaly of the trisomy 16 mouse.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 86 citations in OpenAlex.
- 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
- Neurodevelopmental disorders and microcephaly: how apoptosis, the cell cycle, tau and amyloid-β precursor protein APPly.Frontiers in molecular neuroscience · 2023Review
- Enhanced GIRK2 channel signaling in Down syndrome: A feasible role in the development of abnormal nascent neural circuits.Frontiers in genetics · 2022Review
- Article
- Down syndrome is accompanied by significantly reduced cortical grey-white matter tissue contrast.Human brain mapping · 2018Article
- Mathematical Modeling of Cortical Neurogenesis Reveals that the Founder Population does not Necessarily Scale with Neurogenic Output.Cerebral cortex (New York, N.Y. : 1991) · 2018Article
- Lifespan analysis of brain development, gene expression and behavioral phenotypes in the Ts1Cje, Ts65Dn and Dp(16)1/Yey mouse models of Down syndrome.Disease models & mechanisms · 2018Article
- Histology Atlas of the Developing Prenatal and Postnatal Mouse Central Nervous System, with Emphasis on Prenatal Days E7.5 to E18.5.Toxicologic pathology · 2017Article
- Absence of Prenatal Forebrain Defects in the Dp(16)1Yey/+ Mouse Model of Down Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- New Perspectives for the Rescue of Cognitive Disability in Down Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Modeling local and cross-species neuron number variations in the cerebral cortex as arising from a common mechanism.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- An adaptive threshold in mammalian neocortical evolution.PLoS biology · 2014Article
- The amyloid precursor protein (APP) triplicated gene impairs neuronal precursor differentiation and neurite development through two different domains in the Ts65Dn mouse model for Down syndrome.The Journal of biological chemistry · 2013Article
- Deficits in human trisomy 21 iPSCs and neurons.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Commonality in Down and fetal alcohol syndromes.Birth defects research. Part A, Clinical and molecular teratology · 2013Article
- Widespread proliferation impairment and hypocellularity in the cerebellum of fetuses with down syndrome.Brain pathology (Zurich, Switzerland) · 2011Article
- Seeing beyond the average cell: branching process models of cell proliferation, differentiation, and death during mouse brain development.Theory in biosciences = Theorie in den Biowissenschaften · 2011Review
- Abnormal microRNA expression in Ts65Dn hippocampus and whole blood: contributions to Down syndrome phenotypes.Developmental neuroscience · 2011Article
- Gene network disruptions and neurogenesis defects in the adult Ts1Cje mouse model of Down syndrome.PloS one · 2010Article
- Early pharmacotherapy restores neurogenesis and cognitive performance in the Ts65Dn mouse model for Down syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Development of the neocortex of the trisomy 16 (Ts16) mouse, an animal model of Down syndrome (DS), is characterized by a transient delay in the radial expansion of the cortical wall and a persistent reduction in cortical volume. Here we show that at each cell cycle during neuronogenesis, a smaller proportion of Ts16 progenitors exit the cell cycle than do control, euploid progenitors. In addition, the cell cycle duration was found to be longer in Ts16 than in euploid progenitors, the Ts16 growth fraction was reduced, and an increase in apoptosis was observed in both proliferative and postmitotic zones of the developing Ts16 neocortical wall. Incorporation of these changes into a model of neuronogenesis indicates that they are sufficient to account for the observed delay in radial expansion. In addition, the number of neocortical founder cells, i.e., precursors present just before neuronogenesis begins, is reduced by 26% in Ts16 mice, leading to a reduction in overall cortical size at the end of Ts16 neuronogenesis. Thus, altered proliferative characteristics during Ts16 neuronogenesis result in a delay in the generation of neocortical neurons, whereas the founder cell deficit leads to a proportional reduction in the overall number of neurons. Such prenatal perturbations in either the timing of neuron generation or the final number of neurons produced may lead to significant neocortical abnormalities such as those found in DS.
Indexed as
Identifiers
10818151PMC6772637W1884108341What OpenQuestion holds
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.