ArticleGenetics2014
Cognition and hippocampal plasticity in the mouse is altered by monosomy of a genomic region implicated in Down syndrome.
Article in Genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- N7-methylguanosine modification in cancers: from mechanisms to therapeutic potential.Journal of hematology & oncology · 2025Review
- Liquid-liquid phase separation in diseases.MedComm · 2024Review
- Internal m7G methylation: A novel epitranscriptomic contributor in brain development and diseases.Molecular therapy. Nucleic acids · 2023Review
- Rodent models in Down syndrome research: impact and future opportunities.Disease models & mechanisms · 2017Review
- Genetic Polymorphism of GABRR2 Modulates Individuals' General Cognitive Ability in Healthy Chinese Han People.Cellular and molecular neurobiology · 2017Article
- Down Syndrome Developmental Brain Transcriptome Reveals Defective Oligodendrocyte Differentiation and Myelination.Neuron · 2016Article
- Cognitive Impairment, Neuroimaging, and Alzheimer Neuropathology in Mouse Models of Down Syndrome.Current Alzheimer research · 2016Review
- A novel cause for primordial dwarfism revealed: defective tRNA modification.Genome biology · 2015Article
- Deletion of the App-Runx1 region in mice models human partial monosomy 21.Disease models & mechanisms · 2015Article
- Stem and progenitor cell dysfunction in human trisomies.EMBO reports · 2015Review
- Down Syndrome Cognitive Phenotypes Modeled in Mice Trisomic for All HSA 21 Homologues.PloS one · 2015Article
- Dosage of the Abcg1-U2af1 region modifies locomotor and cognitive deficits observed in the Tc1 mouse model of Down syndrome.PloS one · 2015Article
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Authors and funding
9 authors at 8 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Down syndrome (DS) is due to increased copy number of human chromosome 21. The contribution of different genetic regions has been tested using mouse models. As shown previously, the Abcg1-U2af1 genetic region contributes to cognitive defects in working and short-term recognition memory in Down syndrome mouse models. Here we analyzed the impact of monosomy of the same genetic interval, using a new mouse model, named Ms2Yah. We used several cognitive paradigms and did not detect defects in the object recognition or the Morris water maze tests. However, surprisingly, Ms2Yah mice displayed increased associative memory in a pure contextual fear-conditioning test and decreased social novelty interaction along with a larger long-term potentiation recorded in the CA1 area following stimulation of Schaffer collaterals. Whole-genome expression studies carried out on hippocampus showed that the transcription of only a small number of genes is affected, mainly from the genetic interval (Cbs, Rsph1, Wdr4), with a few additional ones, including the postsynaptic Gabrr2, Gabbr1, Grid2p, Park2, and Dlg1 and the components of the Ubiquitin-mediated proteolysis (Anapc1, Rnf7, Huwe1, Park2). The Abcg1-U2af1 region is undeniably encompassing dosage-sensitive genes or elements whose change in copy number directly affects learning and memory, synaptic function, and autistic related behavior.
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