ArticlePloS one2011
S100B and APP promote a gliocentric shift and impaired neurogenesis in Down syndrome neural progenitors.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 91 citations in OpenAlex.
- Amyloid precursor protein dosage normalization rescues neurogenesis and Alzheimer's Disease phenotypes associated with Down Syndrome.Medical research archives · 2026Article
- A modified CRISPR/Cas9 approach in silencing the triplication in Down syndrome: A treatment path XISTs.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Accelerated Tempo of Cortical Neurogenesis in Down Syndrome.bioRxiv : the preprint server for biology · 2025Article
- Diverse role of S100 calcium-binding protein B in alzheimer's disease: pathological mechanisms and therapeutic implications.Inflammopharmacology · 2025Review
- The restoration of REST inhibits reactivity of Down syndrome iPSC-derived astrocytes.Frontiers in molecular neuroscience · 2025Article
- Brain volumes, cognitive, and adaptive skills in school-age children with Down syndrome.Journal of neurodevelopmental disorders · 2024Article
- Changes in Astroglial Water Flow in the Pre-amyloid Phase of the STZ Model of AD Dementia.Neurochemical research · 2024Article
- A dynamic in vitro model of Down syndrome neurogenesis with trisomy 21 gene dosage correction.Science advances · 2024Article
- The Role of Oxidative Stress in Trisomy 21 Phenotype.Cellular and molecular neurobiology · 2023Review
- Astrocytes in human central nervous system diseases: a frontier for new therapies.Signal transduction and targeted therapy · 2023Review
- Brain Mitochondrial Bioenergetics in Genetic Neurodevelopmental Disorders: Focus on Down, Rett and Fragile X Syndromes.International journal of molecular sciences · 2023Review
- Article
- 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
- Neurogenesis and neuronal differentiation in the postnatal frontal cortex in Down syndrome.Acta neuropathologica communications · 2022Article
- Prenatal and Postnatal Pharmacotherapy in Down Syndrome: The Search to Prevent or Ameliorate Neurodevelopmental and Neurodegenerative Disorders.Annual review of pharmacology and toxicology · 2022Article
- Rodent Modeling of Alzheimer's Disease in Down Syndrome:Frontiers in neuroscience · 2022Review
- Large-scale organoid study suggests effects of trisomy 21 on early fetal neurodevelopment are more subtle than variability between isogenic lines and experiments.Frontiers in neuroscience · 2022Article
- Astroglial and microglial pathology in Down syndrome: Focus on Alzheimer's disease.Frontiers in cellular neuroscience · 2022Review
- The Challenging Pathway of Treatment for Neurogenesis Impairment in Down Syndrome: Achievements and Perspectives.Frontiers in cellular neuroscience · 2022Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
Down syndrome (DS) is a developmental disorder associated with mental retardation (MR) and early onset Alzheimer's disease (AD). These CNS phenotypes are attributed to ongoing neuronal degeneration due to constitutive overexpression of chromosome 21 (HSA21) genes. We have previously shown that HSA21 associated S100B contributes to oxidative stress and apoptosis in DS human neural progenitors (HNPs). Here we show that DS HNPs isolated from fetal frontal cortex demonstrate not only disturbances in redox states within the mitochondria and increased levels of progenitor cell death but also transition to more gliocentric progenitor phenotypes with a consequent reduction in neuronogenesis. HSA21 associated S100B and amyloid precursor protein (APP) levels are simultaneously increased within DS HNPs, their secretions are synergistically enhanced in a paracrine fashion, and overexpressions of these proteins disrupt mitochondrial membrane potentials and redox states. HNPs show greater susceptibility to these proteins as compared to neurons, leading to cell death. Ongoing inflammation through APP and S100B overexpression further promotes a gliocentric HNPs phenotype. Thus, the loss in neuronal numbers seen in DS is not merely due to increased HNPs cell death and neurodegeneration, but also a fundamental gliocentric shift in the progenitor pool that impairs neuronal production.
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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.