Defects in Embryonic Neurogenesis and Initial Synapse Formation in the Forebrain of the Ts65Dn Mouse Model of Down Syndrome
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Trisomy 21, one of the most prevalent congenital birth defects, results in a constellation of phenotypes collectively termed Down syndrome (DS). Mental retardation and motor and sensory deficits are among the many debilitating symptoms of DS. Alterations in brain growth and synaptic development are thought to underlie the cognitive impairments in DS, but the role of early brain development has not been studied because of the lack of embryonic human tissue and because of breeding difficulties in mouse models of DS. We generated a breeding colony of the Ts65Dn mouse model of DS to test the hypothesis that early defects in embryonic brain development are a component of brain dysfunction in DS. We found substantial delays in prenatal growth of the Ts65Dn cerebral cortex and hippocampus because of longer cell cycle duration and reduced neurogenesis from the ventricular zone neural precursor population. In addition, the Ts65Dn neocortex remains hypocellular after birth and there is a lasting decrease in synaptic development beginning in the first postnatal week. These results demonstrate that specific abnormalities in embryonic forebrain precursor cells precede early deficits in synaptogenesis and may underlie the postnatal disabilities in Ts65Dn and DS. The early prenatal period is therefore an important new window for possible therapeutic amelioration of the cognitive symptoms in DS.
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In Down syndrome, particular neurodevelopmental events are delayed in forebrain regions such as neurogenesis, migration and synaptogenesis, eventually resulting in altered prefrontal circuitry.
“Particular neurodevelopmental events are delayed in forebrain regions such as neurogenesis, migration and synaptogenesis eventually resulting in altered prefrontal circuitry [294–296].”
From Development of prefrontal cortex (2022) · cites this paper as [294]
The Discussion reports delayed forebrain development and synapse formation in Ts65Dn mice, and the section 'Defects in synapse formation in Ts65Dn and DS forebrain' also describes defects in neurogenesis and migration. The paper suggests similar abnormalities may occur in people with Down syndrome, but it does not establish delayed migration specifically or show that these changes eventually alter prefrontal circuitry. Page numbers were not available in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThough Ts65Dn fails to capture the majority of the volumetric changes observed in humans, they do appear to recapitulate the synaptic changes as decreases in synaptic density have been identified in both the hippocampus and the neocortex.
“Though Ts65Dn fails to capture the majority of the volumetric changes observed in humans, they do appear to recapitulate the synaptic changes as decreases in synaptic density have been identified in both the hippocampus and the neocortex (Belichenko et al., 2004; Chakrabarti et al., 2007).”
From Neurodevelopment in Down syndrome: Concordance in humans and models (2022) · cites this paper as Chakrabarti et al., 2007
The section “Synapse development is impaired in Ts65Dn neocortex and hippocampus” reports fewer synaptic puncta in both regions at P8, supporting the synaptic part of the claim. The paper describes some differences and similarities in brain growth between Ts65Dn mice and humans with Down syndrome, but does not establish that Ts65Dn fails to capture the majority of human volumetric changes. (LLM, conf=0.84)
Experimental — accuracy not yet measuredIncreases in the cell cycle length of neural progenitor cells in the germinal zone of both the dorsal telencephalon and hippocampus have been found in Ts65Dn, resulting in slower proliferation and decreasing the expansion of the progenitor pool.
“Increases in the cell cycle length of NPCs in the germinal zone of both the dorsal telencephalon and hippocampus have been found, resulting in slower proliferation and decreasing the expansion of the progenitor pool (Chakrabarti et al., 2007).”
From Neurodevelopment in Down syndrome: Concordance in humans and models (2022) · cites this paper as Chakrabarti et al., 2007
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Experimental — accuracy not yet measuredUnlike humans, this hypocellularity does not appear to be driving persistent volumetric changes in these structures, as size deficits detected prenatally do not persist postnatally except in the cerebellum.
“However, unlike humans, this hypocellularity does not appear to be driving persistent volumetric changes in these structures, as size deficits detected prenatally (Chakrabarti et al., 2007) do not persist postnatally except in the cerebellum (Baxter et al., 2000; Olson et al., 2004).”
From Neurodevelopment in Down syndrome: Concordance in humans and models (2022) · cites this paper as Chakrabarti et al., 2007
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“of the volumetric changes observed in humans, they do appear to recapitulate the synaptic changes as decreases in synaptic density have been identified in both the hippocampus and the neocortex (Belichenko et al., 2004; Chakrabarti et al., 2007).”
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Biphasic cell cycle defect causes impaired neurogenesis in down syndrome
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Hawley, L. E., Stringer, M., Deal, A. J., Folz, A., Goodlett, C. R., & Roper, R. J. (2024) · Neurobiology of Disease · doi:10.1016/j.nbd.2023.106359 · Cited by 10 · see citing works
“…do exhibit deficient neurological structural phenotypes in brain regions where we found DYRK1A overexpression including during perinatal or early postnatal ages (Baxter et al., 2000; Belichenko et al., 2004; Bianchi et al., 2010; Chakrabarti et al., 2007; Roper et al., 2006b; Stagni et al., 2016).”
Ishihara, K. (2021) · Genes · doi:10.3390/genes12101598 · Cited by 8 · see citing works
Zhou, Y., Tao, L., & Zhu, Y. (2023) · Brain Sciences · doi:10.3390/brainsci13071070 · Cited by 7 · see citing works
- Authors
- Chakrabarti, L., Galdzicki, Z., & Haydar, T. F.
- Affiliations
- Children's National (US)
- Corresponding author
- Haydar, Tarik F.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2007-10-24
- Volume
- 27
- Issue
- 43
- Pages
- 11483-11495
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6673208
- OpenAlex
- W2165432413
- Cited by
- 199
- References
- 74
- Citations by year
- 2026: 6 · 2025: 10 · 2024: 4 · 2023: 12 · 2022: 14 · 2021: 6 · 2020: 7 · 2019: 13 · 2018: 9 · 2017: 8 · 2016: 12 · 2015: 12 · 2014: 8 · 2013: 15 · 2012: 19
- FWCI
- 8.85
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Dana Foundation
- Children's National Hospital
- National Institutes of Health
- Uniformed Services University of the Health Sciences
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD057580, P30HD040677)
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- Down syndrome, Ts65Dn mouse model, embryonic neurogenesis, synaptogenesis, forebrain development, cerebral cortex, hippocampus, cell cycle duration, neural progenitor cells, ventricular zone, cognitive impairment
- MeSH terms
- Animals, Disease Models, Animal, Down Syndrome, Female, Male, Mice, Inbred C57BL, Mice, Transgenic, Neurons, Synapses, Prosencephalon, Embryonic Development, Mice
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