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Cited by 171Down syndrome and intellectual disability researchGenetics and Neurodevelopmental DisordersAlzheimer's disease research and treatments

Mouse models of Down syndrome as a tool to unravel the causes of mental disabilities

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Rueda, Noemí, Flórez, Jesús, Martínez-Cué, Carmen·2012·Neural Plasticity
DOI 10.1155/2012/584071PMC PMC3364589
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Abstract

Down syndrome (DS) is the most common genetic cause of mental disability. Based on the homology of Hsa21 and the murine chromosomes Mmu16, Mmu17 and Mmu10, several mouse models of DS have been developed. The most commonly used model, the Ts65Dn mouse, has been widely used to investigate the neural mechanisms underlying the mental disabilities seen in DS individuals. A wide array of neuromorphological alterations appears to compromise cognitive performance in trisomic mice. Enhanced inhibition due to alterations in GABA A-mediated transmission and disturbances in the glutamatergic, noradrenergic and cholinergic systems, among others, has also been demonstrated. DS cognitive dysfunction caused by neurodevelopmental alterations is worsened in later life stages by neurodegenerative processes. A number of pharmacological therapies have been shown to partially restore morphological anomalies concomitantly with cognition in these mice. In conclusion, the use of mouse models is enormously effective in the study of the neurobiological substrates of mental disabilities in DS and in the testing of therapies that rescue these alterations. These studies provide the basis for developing clinical trials in DS individuals and sustain the hope that some of these drugs will be useful in rescuing mental disabilities in DS individuals.

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  • The Ts65Dn mouse is trisomic for ~100 orthologs of the 364 genes on HSA21 and displays many DS-specific phenotypes, including delays in brain development and cognitive defects.

    “This commonly used DS model is trisomic for ~100 orthologs of the 364 genes on HSA21 and displays many DS-specific phenotypes, including delays in brain development and cognitive defects (Rueda et al., 2012).”

    From Down Syndrome Developmental Brain Transcriptome Reveals Defective Oligodendrocyte Differentiation and Myelination (2016) · cites this paper as Rueda et al., 2012

    Section 2 calls Ts65Dn a commonly used DS model and reports approximately 92 Hsa21-orthologous genes, reasonably close to the claim’s ~100. Sections 3 and 4 describe cognitive deficits and altered early brain development. However, Section 2 gives approximately 552 genes on the long arm of Hsa21, not 364, so the claimed HSA21 gene count is not supported. (LLM, conf=0.90)

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Authors
Rueda, N., Flórez, J., & Martínez-Cué, C.
Affiliations
  • Department of Physiology and Pharmacology, Faculty of Medicine, University of Cantabria, Santander 39011, Spain
  • Universidad de Cantabria (ES)
ORCID
Flórez, Jesús
Venue
Neural Plasticity
Publisher
Wiley
Published
2012
Volume
2012
Pages
1-26
ISSN
  • 1687-5443 (ISSN-L)
  • 2090-5904
DOI
10.1155/2012/584071
PMC
PMC3364589
OpenAlex
W2034143722
Cited by
171
References
25
Citations by year
2026: 3 · 2025: 8 · 2024: 13 · 2023: 6 · 2022: 13 · 2021: 16 · 2020: 16 · 2019: 10 · 2018: 12 · 2017: 22 · 2016: 15 · 2015: 9 · 2014: 17 · 2013: 6 · 2012: 5
FWCI
1.85
Type
journal article
Language
en
Open access
Licence
Locations
  • Neural Plasticity (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • UCrea (University of Cantabria) (publishedVersion, cc-by)
  • LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Fondation Jérôme Lejeune (11061012, BFU2008-04397, BFU2011-24755)
  • Spanish Ministry of Innovation and Science (11061012, BFU2008-04397, BFU2011-24755)
Topics
  • Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Down syndrome and intellectual disability research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Keywords
Down syndrome, mouse model, Ts65Dn mouse model, trisomy, intellectual disability, cognitive impairment, GABAergic inhibition, glutamatergic system, noradrenergic system, cholinergic system, brain development, neurodegeneration, neuronal morphology, pharmacotherapy
MeSH terms
Animals, Mental Disorders, Cognition Disorders, Disease Models, Animal, Down Syndrome, Humans, Mice, Transgenic, Mice

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