ArticleFrontiers in neuroscience2019
Neuronal Cell-Intrinsic Defects in Mouse Models of Down Syndrome.
Article in Frontiers in neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- The Role of the Immunoglobulin Superfamily of Cell Adhesion Molecules in Intellectual Disability.Cells · 2026Review
- Interferon signaling modulates Down syndrome-associated Alzheimer's disease pathology in a mouse model.iScience · 2025Article
- Toward the Identification of Neurophysiological Biomarkers for Alzheimer's Disease in Down Syndrome: A Potential Role for Cross-Frequency Phase-Amplitude Coupling Analysis.Aging and disease · 2023Review
- Cell type characterization of spatiotemporal gene co-expression modules in Down syndrome brain.iScience · 2023Article
- Altered cell and RNA isoform diversity in aging Down syndrome brains.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- miR-7b-3p Exerts a Dual Role After Spinal Cord Injury, by Supporting Plasticity and Neuroprotection at Cortical Level.Frontiers in molecular biosciences · 2021Article
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Authors and funding
7 authors.
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Abstract
Down Syndrome (DS) is the most common genetic disorder associated with intellectual disability (ID). Excitatory neurons of DS patients and mouse models show decreased size of dendritic field and reduction of spine density. Whether these defects are caused by cell autonomous alterations or by abnormal multicellular circuitry is still unknown. In this work, we explored this issue by culturing cortical neurons obtained from two mouse models of DS: the widely used Ts65Dn and the less characterized Ts2Cje. We observed that, in the
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