ReviewNeural plasticity2012
From abnormal hippocampal synaptic plasticity in down syndrome mouse models to cognitive disability in down syndrome.
Review in Neural plasticity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 53 citations in OpenAlex.
- Trial
- Memory processing in neurodevelopmental disorders: linking behavioral, circuits, and molecular scales.Frontiers in cellular neuroscience · 2026Review
- Neurodevelopmental Abnormalities in Down Syndrome: Assessing Structural and Functional Deficits.Cureus · 2024Review
- EEG in Down Syndrome-A Review and Insights into Potential Neural Mechanisms.Brain sciences · 2024Review
- Cell type characterization of spatiotemporal gene co-expression modules in Down syndrome brain.iScience · 2023Article
- Glutamatergic synaptic deficits in the prefrontal cortex of the Ts65Dn mouse model for Down syndrome.Frontiers in neuroscience · 2023Article
- GnRH replacement rescues cognition in Down syndrome.Science (New York, N.Y.) · 2022Article
- Sleep-disordered breathing and sleep macro- and micro-architecture in children with Down syndrome.Pediatric research · 2022Article
- Enhanced GIRK2 channel signaling in Down syndrome: A feasible role in the development of abnormal nascent neural circuits.Frontiers in genetics · 2022Review
- Beta-amyloid pore linked to controlled calcium influx into the cell: A new paradigm for Alzheimer's Disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022Article
- Dyrk1a gene dosage in glutamatergic neurons has key effects in cognitive deficits observed in mouse models of MRD7 and Down syndrome.PLoS genetics · 2021Article
- Spaced training improves learning in Ts65Dn and Ube3a mouse models of intellectual disabilities.Translational psychiatry · 2019Article
- Human Models Are Needed for Studying Human Neurodevelopmental Disorders.American journal of human genetics · 2018Review
- Touchscreen learning deficits in Ube3a, Ts65Dn and Mecp2 mouse models of neurodevelopmental disorders with intellectual disabilities.Genes, brain, and behavior · 2018Article
- Phosphoproteomic Alterations of Ionotropic Glutamate Receptors in the Hippocampus of the Ts65Dn Mouse Model of Down Syndrome.Frontiers in molecular neuroscience · 2018Article
- Early neurotrophic pharmacotherapy rescues developmental delay and Alzheimer's-like memory deficits in the Ts65Dn mouse model of Down syndrome.Scientific reports · 2017Article
- Synaptopathies: synaptic dysfunction in neurological disorders - A review from students to students.Journal of neurochemistry · 2016Review
- Hippocampal Wnt Signaling: Memory Regulation and Hormone Interactions.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2016Review
- The Current Status of Somatostatin-Interneurons in Inhibitory Control of Brain Function and Plasticity.Neural plasticity · 2016Review
- Altered intrinsic and network properties of neocortical neurons in the Ts65Dn mouse model of Down syndrome.Physiological reports · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Down syndrome (DS) is caused by the overexpression of genes on triplicated regions of human chromosome 21 (Hsa21). While the resulting physiological and behavioral phenotypes vary in their penetrance and severity, all individuals with DS have variable but significant levels of cognitive disability. At the core of cognitive processes is the phenomenon of synaptic plasticity, a functional change in the strength at points of communication between neurons. A wide variety of evidence from studies on DS individuals and mouse models of DS indicates that synaptic plasticity is adversely affected in human trisomy 21 and mouse segmental trisomy 16, respectively, an outcome that almost certainly extensively contributes to the cognitive impairments associated with DS. In this review, we will highlight some of the neurophysiological changes that we believe reduce the ability of trisomic neurons to undergo neuroplasticity-related adaptations. We will focus primarily on hippocampal networks which appear to be particularly impacted in DS and where consequently the majority of cellular and neuronal network research has been performed using DS animal models, in particular the Ts65Dn mouse. Finally, we will postulate on how altered plasticity may contribute to the DS cognitive disability.
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What OpenQuestion holds
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.