Genes Associated with Disturbed Cerebral Neurogenesis in the Embryonic Brain of Mouse Models of Down Syndrome
Open accessAbstract
Down syndrome (DS), also known as trisomy 21, is the most frequent genetic cause of intellectual disability. Although the mechanism remains unknown, delayed brain development is assumed to be involved in DS intellectual disability. Analyses with human with DS and mouse models have shown that defects in embryonic cortical neurogenesis may lead to delayed brain development. Cre-loxP-mediated chromosomal engineering has allowed the generation of a variety of mouse models carrying various partial Mmu16 segments. These mouse models are useful for determining genotype–phenotype correlations and identifying dosage-sensitive genes involved in the impaired neurogenesis. In this review, we summarize several candidate genes and pathways that have been linked to defective cortical neurogenesis in DS.
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Mouse models have allowed advances in deciphering mechanisms governing brain development and function and the consequences of Down syndrome-related manipulations.
“These models have allowed the scientific community to make incredible advances in deciphering the mechanisms governing brain development and function, as well as the consequences of DS-related manipulations for those mechanisms18–22.”
From Consequences of trisomy 21 for brain development in Down syndrome (2024) · cites this paper as [19]
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- Authors
- Ishihara, K.
- Affiliations
- Kyoto Pharmaceutical University (JP)
- Corresponding author
- Ishihara, Keiichi
- ORCID
- Ishihara, Keiichi
- Venue
- Genes
- Publisher
- MDPI AG
- Published
- 2021-10-11
- Volume
- 12
- Issue
- 10
- Pages
- 1598
- ISSN
- 2073-4425 (ISSN-L)
- PMC
- PMC8535956
- OpenAlex
- W3207063312
- Cited by
- 8
- References
- 84
- Citations by year
- 2026: 2 · 2024: 2 · 2023: 3 · 2022: 1
- FWCI
- 0.27
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Genes (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Takeda Science Foundation (2016 to KI)
- JSPS KAKENHI (18K06940)
- Vehicle Racing Commemorative Foundation (2017 to KI)
- Kyoto Pharmaceutical University Fund for the Promotion of Scientific Research (to KI)
- 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, cortical neurogenesis, embryonic brain development, intellectual disability, mouse model, dosage-sensitive genes, genotype-phenotype correlation, Cre-loxP recombination
- MeSH terms
- Animals, Brain, Cerebellar Cortex, Disease Models, Animal, Down Syndrome, Genotype, Humans, Animals, Genetically Modified, Embryonic Development, Mice, Neurogenesis
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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