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Cited by 29Down syndrome and intellectual disability researchNeurogenesis and neuroplasticity mechanismsFetal and Pediatric Neurological Disorders

Assessment of radial glia in the frontal lobe of fetuses with Down syndrome

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Baburamani, Ana A., Vontell, Regina T., Uus, Alena, Pietsch, Maximilian, Patkee, Prachi A., Wyatt-Ashmead, Jo, Chin-Smith, Evonne C., Supramaniam, Veena G. +3 more·2020·Acta Neuropathologica Communications
DOI 10.1186/s40478-020-01015-3PMC PMC7441567
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Abstract

Down syndrome (DS) occurs with triplication of human chromosome 21 and is associated with deviations in cortical development evidenced by simplified gyral appearance and reduced cortical surface area. Radial glia are neuronal and glial progenitors that also create a scaffolding structure essential for migrating neurons to reach cortical targets and therefore play a critical role in cortical development. The aim of this study was to characterise radial glial expression pattern and morphology in the frontal lobe of the developing human fetal brain with DS and age-matched controls. Secondly, we investigated whether microstructural information from in vivo magnetic resonance imaging (MRI) could reflect histological findings from human brain tissue samples. Immunohistochemistry was performed on paraffin-embedded human post-mortem brain tissue from nine fetuses and neonates with DS (15–39 gestational weeks (GW)) and nine euploid age-matched brains (18–39 GW). Radial glia markers CRYAB, HOPX, SOX2, GFAP and Vimentin were assessed in the Ventricular Zone, Subventricular Zone and Intermediate Zone. In vivo diffusion MRI was used to assess microstructure in these regions in one DS (21 GW) and one control (22 GW) fetal brain. We found a significant reduction in radial glial progenitor SOX2 and subtle deviations in radial glia expression (GFAP and Vimentin) prior to 24 GW in DS. In vivo, fetal MRI demonstrates underlying radial projections consistent with immunohistopathology. Radial glial alterations may contribute to the subsequent simplified gyral patterns and decreased cortical volumes observed in the DS brain. Recent advances in fetal MRI acquisition and analysis could provide non-invasive imaging-based biomarkers of early developmental deviations.

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  • Gross anatomical differences in brain structure are apparent in fetal and neonatal brains of individuals with Down syndrome, including reductions in overall brain volume, white matter volume, gyral complexity, sulcal depth and growth of the cortical plate.

    “Gross anatomical differences in brain structure are apparent in the fetal and neonatal brains of individuals with DS, including reductions in overall brain volume, white matter volume, gyral complexity, sulcal depth and growth of the cortical plate6,8–15.”

    From Consequences of trisomy 21 for brain development in Down syndrome (2024) · cites this paper as [11]

    Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

    Experimental — accuracy not yet measured

  • The number of progenitors, identified by their expression of the transcription factor SOX2, is reduced in post-mortem brain tissue from individuals with Down syndrome.

    “Furthermore, the number of progenitors, identified by their expression of the transcription factor SOX2, is also reduced in post-mortem brain tissue from individuals with DS11.”

    From Consequences of trisomy 21 for brain development in Down syndrome (2024) · cites this paper as [11]

    The Results report fewer SOX2-positive cells in the outer subventricular zone of Down syndrome fetal brains than in age-matched controls. The claim omits that this finding concerns a specific region and gestational period; the Discussion also calls it inconclusive because of the small number of cases. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

  • The presence of fewer cycling cells and the reduced number of progenitors both support the suggestion that neurogenesis is reduced during development in Down syndrome, although these data do not distinguish between slower progenitor proliferation or premature progenitor cell cycle exit.

    “Together, the presence of fewer cycling cells and the reduced number of progenitors both support the suggestion that neurogenesis is reduced during development in DS, although these data do not distinguish between slower progenitor proliferation or premature progenitor cell cycle exit.”

    From Consequences of trisomy 21 for brain development in Down syndrome (2024) · cites this paper as [11]

    Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

    Experimental — accuracy not yet measured

  • Reduced proliferation appears to result in a smaller neural progenitor cell pool, as fewer SOX2+ cells have been reported in the outer subventricular zone in the developing cerebral cortex in fetuses with Down syndrome during mid-gestation (18-24 weeks), potentially limiting the production of neurons and glia.

    “This reduced proliferation appears to result in a smaller NPC pool as fewer SOX2+ cells have been reported in the outer subventricular zone (oSVZ) in the developing cerebral cortex in fetuses with DS during mid-gestation (18–24 weeks) potentially limiting the production of neurons and glia (Baburamani et al., 2020).”

    From Neurodevelopment in Down syndrome: Concordance in humans and models (2022) · cites this paper as Baburamani et al., 2020

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References 66 · Cited by 29

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Authors
Baburamani, A. A., Vontell, R. T., Uus, A., Pietsch, M., Patkee, P. A., Wyatt-Ashmead, J., Chin-Smith, E. C., Supramaniam, V. G., Donald Tournier, J., Deprez, M., & Rutherford, M. A.
Affiliations
  • King's College London (GB)
  • University of Miami (US)
Corresponding author
Baburamani, Ana A.
ORCID
Venue
Acta Neuropathologica Communications
Publisher
Springer Science and Business Media LLC
Published
2020-08-20
Volume
8
Issue
1
Pages
141-141
ISSN
2051-5960 (ISSN-L)
DOI
10.1186/s40478-020-01015-3
PMC
PMC7441567
OpenAlex
W3054210132
Cited by
29
References
66
Citations by year
2026: 2 · 2025: 3 · 2024: 9 · 2023: 6 · 2022: 6 · 2021: 3
FWCI
2.81
Type
journal article
Language
en
Open access
Licence
Locations
  • Acta Neuropathologica Communications (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Medical Research Council UK (MR/K006355)
  • Rosetrees Trust (A1563)
  • Great Ormond Street Hospital Charity (V5318)
  • Sparks Childrens Charity (V5318)
  • Wellcome Trust (WT 203148/Z/16/Z)
  • Engineering and Physical Sciences Research Council (WT 203148/Z/16/)
Topics
  • Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Down syndrome and intellectual disability research
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Fetal and Pediatric Neurological Disorders
Keywords
Down syndrome, radial glia, fetal brain development, frontal lobe, SOX2, cortical development, diffusion MRI, fetal MRI, immunohistochemistry, ventricular zone, subventricular zone, intermediate zone
MeSH terms
Down Syndrome, Female, Fetus, Frontal Lobe, Humans, Infant, Newborn, Male, Neurogenesis, Ependymoglial Cells

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