ArticleBrain pathology (Zurich, Switzerland)2008
Neurogenesis impairment and increased cell death reduce total neuron number in the hippocampal region of fetuses with Down syndrome.
Article in Brain pathology (Zurich, Switzerland), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers, 1 of them a synthesis that pooled it.
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Who cites it
154 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Meta-Analysis of Down Syndrome Cortical Development Reveals Underdeveloped State of the Science.Frontiers in cellular neuroscience · 2022Pooled it
- Down syndrome and dementia: a randomized, controlled trial of antioxidant supplementation.American journal of medical genetics. Part A · 2011Trial
- Fasudil induces anti-inflammatory transcriptomic changes and increased proliferation in human trisomy 21 neural progenitor cells.Biology open · 2026Article
- Article
- 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
- Anti-inflammatory and pro-proliferative effects of fasudil in human trisomy 21 neural progenitor cells.bioRxiv : the preprint server for biology · 2026Article
- Preventing Differentiation Towards Primitive Macrophages in Stem Cells With Down Syndrome.Immunology · 2026Article
- The Wnt/β-catenin pathway maintains homeostasis of amniocytes in Down syndrome.BMC molecular and cell biology · 2026Article
- Chronic suppression of monoacylglycerol lipase restores adult neurogenesis in the septal but not the temporal DG in Ts65Dn mouse model of Down syndrome.Brain research bulletin · 2026Article
- Progenitor diversity during formation of the mammalian neocortex.Frontiers in neuroscience · 2026Review
- Periodontitis and Alzheimer's disease, common pathways in down syndrome.Frontiers in dental medicine · 2026Review
- The placental effects of trisomy for human chromosome 21 orthologs in four mouse models of Down syndrome.Biology open · 2025Article
- Generational effects in Down syndrome: Enriched environment enhances functionality without reducing Alzheimer's disease risk.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Molecular cartography of the human down syndrome and trisomic mouse brain.Nature communications · 2025Article
- Astrocytopathy Is Associated with CA1 Synaptic Dysfunction in a Mouse Model of Down Syndrome.Cells · 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
- Exploratory analysis of the proteomic profile in plasma in adults with Down syndrome in the context of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- A Comprehensive Review on Utilizing Human Brain Organoids to Study Neuroinflammation in Neurological Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Review
94 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously obtained evidence for reduced cell proliferation in the dentate gyrus (DG) of fetuses with Down syndrome (DS), suggesting that the hippocampal hypoplasia seen in adulthood may be caused by defective early neuron production. The goal of this study was to establish whether DS fetuses (17-21 weeks of gestation) exhibit reduction in total cell number in the DG, hippocampus and parahippocampal gyrus (PHG). Volumes of the cellular layers and cell number were estimated with Cavalieri's principle and the optical fractionator method, respectively. We found that in DS fetuses all investigated structures had a reduced volume and cell number. Analysis of cell phenotype showed that DS fetuses had a higher percentage of cells with astrocytic phenotype but a smaller percentage of cells with neuronal phenotype. Immunohistochemistry for Ki-67, a marker of cycling cells, showed that DS fetuses had less proliferating cells in the germinal zones of the hippocampus and PHG. We additionally found that in the hippocampal region of DS fetuses there was a higher incidence of apoptotic cell death. Results show reduced neuron number in the DS hippocampal region and suggest that this defect is caused by disruption of neurogenesis and apoptosis, two fundamental processes underlying brain building.
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