ArticlePloS one2010
Gene network disruptions and neurogenesis defects in the adult Ts1Cje mouse model of Down syndrome.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 58 citations in OpenAlex.
- Helicid Alleviates Neuronal Apoptosis of Rats with Depression-Like Behaviors by Downregulating lncRNA-NONRATT030918.2.Molecular neurobiology · 2024Article
- Regulation of young-adult neurogenesis and neuronal differentiation by neural cell adhesion molecule 2 (NCAM2).Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- Article
- The microRNA-17 ~ 92 Family as a Key Regulator of Neurogenesis and Potential Regenerative Therapeutics of Neurological Disorders.Stem cell reviews and reports · 2022Review
- Gene alteration in zebrafish exposed to a mixture of substances of abuse.Environmental pollution (Barking, Essex : 1987) · 2021Article
- Transient prenatal ruxolitinib treatment suppresses astrogenesis during development and improves learning and memory in adult mice.Scientific reports · 2021Article
- Phenotype microarrays reveal metabolic dysregulations of neurospheres derived from embryonic Ts1Cje mouse model of Down syndrome.PloS one · 2020Article
- Expression Profiling of Notch Signalling Pathway and Gamma-Secretase Activity in the Brain of Ts1Cje Mouse Model of Down Syndrome.Journal of molecular neuroscience : MN · 2019Article
- Potential Role of JAK-STAT Signaling Pathway in the Neurogenic-to-Gliogenic Shift in Down Syndrome Brain.Neural plasticity · 2016Review
- Analysis of adult cerebral cortex and hippocampus transcriptomes reveals unique molecular changes in the Ts1Cje mouse model of down syndrome.Brain pathology (Zurich, Switzerland) · 2015Article
- A three-dimensional collagen construct to model lipopolysaccharide-induced activation of BV2 microglia.Journal of neuroinflammation · 2014Article
- Functional transcriptome analysis of the postnatal brain of the Ts1Cje mouse model for Down syndrome reveals global disruption of interferon-related molecular networks.BMC genomics · 2014Article
- Dosage of Dyrk1a shifts cells within a p21-cyclin D1 signaling map to control the decision to enter the cell cycle.Molecular cell · 2013Article
- The amyloid precursor protein (APP) triplicated gene impairs neuronal precursor differentiation and neurite development through two different domains in the Ts65Dn mouse model for Down syndrome.The Journal of biological chemistry · 2013Article
- Global DNA hypermethylation in down syndrome placenta.PLoS genetics · 2013Article
- OLIG2 over-expression impairs proliferation of human Down syndrome neural progenitors.Human molecular genetics · 2012Article
- Molecular and cellular alterations in Down syndrome: toward the identification of targets for therapeutics.Neural plasticity · 2012Review
- Mouse models of Down syndrome as a tool to unravel the causes of mental disabilities.Neural plasticity · 2012Review
- Widespread proliferation impairment and hypocellularity in the cerebellum of fetuses with down syndrome.Brain pathology (Zurich, Switzerland) · 2011Article
- DYRK1A protein kinase promotes quiescence and senescence through DREAM complex assembly.Genes & development · 2011Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDown syndrome (DS) individuals suffer mental retardation with further cognitive decline and early onset Alzheimer's disease. METHODOLOGY/PRINCIPAL
findingsTo understand how trisomy 21 causes these neurological abnormalities we investigated changes in gene expression networks combined with a systematic cell lineage analysis of adult neurogenesis using the Ts1Cje mouse model of DS. We demonstrated down regulation of a number of key genes involved in proliferation and cell cycle progression including Mcm7, Brca2, Prim1, Cenpo and Aurka in trisomic neurospheres. We found that trisomy did not affect the number of adult neural stem cells but resulted in reduced numbers of neural progenitors and neuroblasts. Analysis of differentiating adult Ts1Cje neural progenitors showed a severe reduction in numbers of neurons produced with a tendency for less elaborate neurites, whilst the numbers of astrocytes was increased. CONCLUSIONS/SIGNIFICANCE: We have shown that trisomy affects a number of elements of adult neurogenesis likely to result in a progressive pathogenesis and consequently providing the potential for the development of therapies to slow progression of, or even ameliorate the neuronal deficits suffered by DS individuals.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.