The "Down syndrome critical region" is sufficient in the mouse model to confer behavioral, neurophysiological, and synaptic phenotypes characteristic of Down syndrome
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Down syndrome: searching for the genetic culpritsProspects for Improving Brain Function in Individuals with Down SyndromeEmerging pharmacotherapies for neurodevelopmental disordersBehavioral and Genetic Evidence for GIRK Channels in the CNS: Role in Physiology, Pathophysiology, and Drug AddictionMouse models of Down syndrome as a tool to unravel the causes of mental disabilitiesDendritic spine dysgenesis in autism related disordersAlzheimer's disease therapeutics targeted to the control of amyloid precursor protein translation: maintenance of brain iron homeostasisDown Syndrome Cognitive Phenotypes Modeled in Mice Trisomic for All HSA 21 HomologuesHippocampal circuit dysfunction in the Tc1 mouse model of Down syndrome.The DCR protein TTC3 affects differentiation and Golgi compactness in neurons through specific actin-regulating pathwaysSynaptopathies: synaptic dysfunction in neurological disorders - A review from students to studentsAnimal models of intellectual disability: towards a translational approachDSCR1 interacts with FMRP and is required for spine morphogenesis and local protein synthesisDosage of the Abcg1-U2af1 region modifies locomotor and cognitive deficits observed in the Tc1 mouse model of Down syndromeComprehensive behavioral phenotyping of Ts65Dn mouse model of Down syndrome: activation of β1-adrenergic receptor by xamoterol as a potential cognitive enhancer.The use of mouse models to understand and improve cognitive deficits in Down syndrome.PCP4 (PEP19) overexpression induces premature neuronal differentiation associated with Ca(2+) /calmodulin-dependent kinase II-δ activation in mouse models of Down syndrome.Genetic dissection of the Down syndrome critical region.Molecular basis of pharmacotherapies for cognition in Down syndromeModulation of GABAergic transmission in development and neurodevelopmental disorders: investigating physiology and pathology to gain therapeutic perspectives.Global gene expression profiling of somatic motor neuron populations with different vulnerability identify molecules and pathways of degeneration and protectionMeeting at the crossroads: common mechanisms in Fragile X and Down syndromeFunctional transcriptome analysis of the postnatal brain of the Ts1Cje mouse model for Down syndrome reveals global disruption of interferon-related molecular networksMaternal choline supplementation improves spatial mapping and increases basal forebrain cholinergic neuron number and size in aged Ts65Dn mice.An easy and versatile 2-step protocol for targeted modification and subcloning of DNA from bacterial artificial chromosomes using non-commercial plasmids.Maternal choline supplementation programs greater activity of the phosphatidylethanolamine N-methyltransferase (PEMT) pathway in adult Ts65Dn trisomic miceExpression profile analysis of vulnerable CA1 pyramidal neurons in young-Middle-Aged Ts65Dn mice.Expression profile analysis of hippocampal CA1 pyramidal neurons in aged Ts65Dn mice, a model of Down syndrome (DS) and Alzheimer's disease (AD).Alterations to dendritic spine morphology, but not dendrite patterning, of cortical projection neurons in Tc1 and Ts1Rhr mouse models of Down syndromeThe Down syndrome critical region regulates retinogeniculate refinementDisruption of neurogenesis and cortical development in transgenic mice misexpressing Olig2, a gene in the Down syndrome critical regionTrisomic and allelic differences influence phenotypic variability during development of Down syndrome mice.Mouse models for Down syndrome-associated developmental cognitive disabilitiesIncreased efficiency of the GABAA and GABAB receptor-mediated neurotransmission in the Ts65Dn mouse model of Down syndromeTrisomy 21 and early brain developmentAltered synaptic marker abundance in the hippocampal stratum oriens of Ts65Dn mice is associated with exuberant expression of versicanTrisomy of the G protein-coupled K+ channel gene, Kcnj6, affects reward mechanisms, cognitive functions, and synaptic plasticity in mice.Age-related neurodegeneration and memory loss in down syndrome.Thy1-hAPP(Lond/Swe+) mouse model of Alzheimer's disease displays broad behavioral deficits in sensorimotor, cognitive and social functionMolecular and cellular alterations in Down syndrome: toward the identification of targets for therapeutics
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The "Down syndrome critical region" is sufficient in the mouse model to confer behavioral, neurophysiological, and synaptic phenotypes characteristic of Down syndrome
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
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scientific article published on May 2009
@en
vedecký článok
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vetenskaplig artikel
@sv
videnskabelig artikel
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vědecký článek
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name
The "Down syndrome critical re ...... haracteristic of Down syndrome
@en
The "Down syndrome critical re ...... aracteristic of Down syndrome.
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type
label
The "Down syndrome critical re ...... haracteristic of Down syndrome
@en
The "Down syndrome critical re ...... aracteristic of Down syndrome.
@nl
prefLabel
The "Down syndrome critical re ...... haracteristic of Down syndrome
@en
The "Down syndrome critical re ...... aracteristic of Down syndrome.
@nl
P2093
P2860
P1476
The "Down syndrome critical re ...... haracteristic of Down syndrome
@en
P2093
Nadia P Belichenko
Pavel V Belichenko
Roger H Reeves
William C Mobley
P2860
P304
P356
10.1523/JNEUROSCI.1547-09.2009
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P577
2009-05-01T00:00:00Z