ReviewCells2019
Aberrant Oligodendrogenesis in Down Syndrome: Shift in Gliogenesis?
Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed.
- Periodontitis and Alzheimer's disease, common pathways in down syndrome.Frontiers in dental medicine · 2026Review
- Accelerated Tempo of Cortical Neurogenesis in Down Syndrome.bioRxiv : the preprint server for biology · 2025Article
- Reversing intellectual disabilities in Down syndrome: Hopes or hypes?The Indian journal of medical research · 2025Article
- Pros and Cons of Human Brain Organoids to Study Alzheimer's Disease.Aging and disease · 2024Review
- Consequences of trisomy 21 for brain development in Down syndrome.Nature reviews. Neuroscience · 2024Review
- Cerebrovascular disease is associated with Alzheimer's plasma biomarker concentrations in adults with Down syndrome.Brain communications · 2024Article
- Article
- Comprehensive volumetric phenotyping of the neonatal brain in Down syndrome.Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- Article
- Extracellular Vesicle Treatment Alleviates Neurodevelopmental and Neurodegenerative Pathology in Cortical Spheroid Model of Down Syndrome.International journal of molecular sciences · 2023Article
- Shaking up the silence: consequences of HMGN1 antagonizing PRC2 in the Down syndrome brain.Epigenetics & chromatin · 2022Review
- The innate immune system stimulating cytokine GM-CSF improves learning/memory and interneuron and astrocyte brain pathology in Dp16 Down syndrome mice and improves learning/memory in wild-type mice.Neurobiology of disease · 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
- Curcumin Ameliorates White Matter Injury after Ischemic Stroke by Inhibiting Microglia/Macrophage Pyroptosis through NF-Oxidative medicine and cellular longevity · 2021Article
- New Insights Into the Roles of Microglial Regulation in Brain Plasticity-Dependent Stroke Recovery.Frontiers in cellular neuroscience · 2021Review
- Unraveling Human Brain Development and Evolution Using Organoid Models.Frontiers in cell and developmental biology · 2021Review
- Rapid and Efficient Generation of Myelinating Human Oligodendrocytes in Organoids.Frontiers in cellular neuroscience · 2021Article
- C21orf91 Regulates Oligodendroglial Precursor Cell Fate-A Switch in the Glial Lineage?Frontiers in cellular neuroscience · 2021Article
- Molecular Mechanisms of Cognitive Impairment and Intellectual Disability-Virtual ESN Mini-Conference in Conjunction with the FENS Forum, July 11-15, 2020.Journal of molecular neuroscience : MN · 2020Article
- Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Down syndrome (DS), or trisomy 21, is the most prevalent chromosomal anomaly accounting for cognitive impairment and intellectual disability (ID). Neuropathological changes of DS brains are characterized by a reduction in the number of neurons and oligodendrocytes, accompanied by hypomyelination and astrogliosis. Recent studies mainly focused on neuronal development in DS, but underestimated the role of glial cells as pathogenic players. Aberrant or impaired differentiation within the oligodendroglial lineage and altered white matter functionality are thought to contribute to central nervous system (CNS) malformations. Given that white matter, comprised of oligodendrocytes and their myelin sheaths, is vital for higher brain function, gathering knowledge about pathways and modulators challenging oligodendrogenesis and cell lineages within DS is essential. This review article discusses to what degree DS-related effects on oligodendroglial cells have been described and presents collected evidence regarding induced cell-fate switches, thereby resulting in an enhanced generation of astrocytes. Moreover, alterations in white matter formation observed in mouse and human post-mortem brains are described. Finally, the rationale for a better understanding of pathways and modulators responsible for the glial cell imbalance as a possible source for future therapeutic interventions is given based on current experience on pro-oligodendroglial treatment approaches developed for demyelinating diseases, such as multiple sclerosis.
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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.