ArticleNature neuroscience2010
Olig1 and Olig2 triplication causes developmental brain defects in Down syndrome.
Article in Nature neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.
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Who cites it
139 citing papers in PubMed, 269 citations in OpenAlex.
- Trial
- Neuid: A Novel Neuron-Enriched LncRNA that Connects Epigenetic Gene Silencing to Alzheimer's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Molecular and cellular processes disrupted in the early postnatal Down syndrome prefrontal cortex.Science (New York, N.Y.) · 2026Article
- Synaptic and intrinsic membrane defects disrupt early neural network dynamics in Down syndrome.Nature communications · 2026Article
- Increased dendritic inhibition of dentate gyrus granule cells in a mouse model of Down syndrome.Frontiers in cellular neuroscience · 2026Article
- Molecular cartography of the human down syndrome and trisomic mouse brain.Nature communications · 2025Article
- Accelerated Tempo of Cortical Neurogenesis in Down Syndrome.bioRxiv : the preprint server for biology · 2025Article
- Article
- The Hallmarks of Aneuploidy in Cancer and Congenital Syndromes.Annual review of genomics and human genetics · 2025Review
- Profiling hippocampal neuronal populations reveals unique gene expression mosaics reflective of connectivity-based degeneration in the Ts65Dn mouse model of Down syndrome and Alzheimer's disease.Frontiers in molecular neuroscience · 2025Article
- The lncRNA Snhg11, a new candidate contributing to neurogenesis, plasticity, and memory deficits in Down syndrome.Molecular psychiatry · 2024Article
- In and out: Benchmarking in vitro, in vivo, ex vivo, and xenografting approaches for an integrative brain disease modeling pipeline.Stem cell reports · 2024Review
- Choroid plexus defects in Down syndrome brain organoids enhance neurotropism of SARS-CoV-2.Science advances · 2024Article
- Gene Expression Studies in Down Syndrome: What Do They Tell Us about Disease Phenotypes?International journal of molecular sciences · 2024Review
- Understanding the genetic mechanisms and cognitive impairments in Down syndrome: towards a holistic approach.Journal of neurology · 2024Review
- Lamivudine modulates the expression of neurological impairment-related genes and LINE-1 retrotransposons in brain tissues of a Down syndrome mouse model.Frontiers in aging neuroscience · 2024Article
- Neocortical neuronal production and maturation defects in the TcMAC21 mouse model of Down syndrome.iScience · 2023Article
- The lncRNA Snhg11, a new candidate contributing to neurogenesis, plasticity and memory deficits in Down syndrome.Research square · 2023Article
- Article
- TempShift Reveals the Sequential Development of Human Neocortex and Skewed Developmental Timing of Down Syndrome Brains.Brain sciences · 2023Article
79 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Over-inhibition is thought to be one of the underlying causes of the cognitive deficits in Ts65Dn mice, the most widely used model of Down syndrome. We found a direct link between gene triplication and defects in neuron production during embryonic development. These neurogenesis defects led to an imbalance between excitatory and inhibitory neurons and to increased inhibitory drive in the Ts65Dn forebrain. We discovered that Olig1 and Olig2, two genes that are triplicated in Down syndrome and in Ts65Dn mice, were overexpressed in the Ts65Dn forebrain. To test the hypothesis that Olig triplication causes the neurological phenotype, we used a genetic approach to normalize the dosage of these two genes and thereby rescued the inhibitory neuron phenotype in the Ts65Dn brain. These data identify seminal alterations during brain development and suggest a mechanistic relationship between triplicated genes and these brain abnormalities in the Ts65Dn mouse.
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Registered trials
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.