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Concise review: new paradigms for Down syndrome research using induced pluripotent stem cells: tackling complex human genetic diseaseDissecting Alzheimer disease in Down syndrome using mouse modelsCyclin D1 Again Caught in the Act: Dyrk1a Links G1 and Neurogenesis in Down SyndromeModeling a model: Mouse genetics, 22q11.2 Deletion Syndrome, and disorders of cortical circuit developmentA 'cure' for Down syndrome: what do parents want?The Down syndrome-related protein kinase DYRK1A phosphorylates p27(Kip1) and Cyclin D1 and induces cell cycle exit and neuronal differentiationFunctional transcriptome analysis of the postnatal brain of the Ts1Cje mouse model for Down syndrome reveals global disruption of interferon-related molecular networksTranslating dosage compensation to trisomy 21Noninvasive prenatal testing creates an opportunity for antenatal treatment of Down syndrome.Dysregulation of protein trafficking in neurodegeneration.Differentially expressed microRNAs in maternal plasma for the noninvasive prenatal diagnosis of Down syndrome (trisomy 21).Acute upregulation of hedgehog signaling in mice causes differential effects on cranial morphology.DSCAM promotes refinement in the mouse retina through cell death and restriction of exploring dendrites.Contribution of copy-number variation to Down syndrome-associated atrioventricular septal defects.Disruption of neurogenesis and cortical development in transgenic mice misexpressing Olig2, a gene in the Down syndrome critical regionProfiles of everyday executive functioning in young children with down syndrome.Identification of a novel actin-dependent signal transducing module allows for the targeted degradation of GLI1Increased excitability and altered action potential waveform in cerebellar granule neurons of the Ts65Dn mouse model of Down syndromeFrom abnormal hippocampal synaptic plasticity in down syndrome mouse models to cognitive disability in down syndrome.Deficits in cognition and synaptic plasticity in a mouse model of Down syndrome ameliorated by GABAB receptor antagonists.Perinatal Choline Supplementation Reduces Amyloidosis and Increases Choline Acetyltransferase Expression in the Hippocampus of the APPswePS1dE9 Alzheimer's Disease Model MiceDYRK1A overexpression enhances STAT activity and astrogliogenesis in a Down syndrome mouse model.RCAN1 links impaired neurotrophin trafficking to aberrant development of the sympathetic nervous system in Down syndrome.Evidence of altered age-related brain cytoarchitecture in mouse models of down syndrome: a diffusional kurtosis imaging studyAbsence of Prenatal Forebrain Defects in the Dp(16)1Yey/+ Mouse Model of Down Syndrome.Down Syndrome Developmental Brain Transcriptome Reveals Defective Oligodendrocyte Differentiation and Myelination.Receptor-interacting protein 140 overexpression promotes neuro-2a neuronal differentiation by ERK1/2 signaling.Weaker control of the electrical properties of cerebellar granule cells by tonically active GABAA receptors in the Ts65Dn mouse model of Down's syndrome.Separated at birth? The functional and molecular divergence of OLIG1 and OLIG2.The HSA21 gene EURL/C21ORF91 controls neurogenesis within the cerebral cortex and is implicated in the pathogenesis of Down SyndromeAn Integrated Human/Murine Transcriptome and Pathway Approach To Identify Prenatal Treatments For Down Syndrome.Dosage of amyloid precursor protein affects axonal contact guidance in Down syndrome.Changing Paradigms in Down Syndrome: The First International Conference of the Trisomy 21 Research Society.Correlation between receptor-interacting protein 140 expression and directed differentiation of human embryonic stem cells into neural stem cells.Early neurotrophic pharmacotherapy rescues developmental delay and Alzheimer's-like memory deficits in the Ts65Dn mouse model of Down syndrome.Stem and progenitor cell dysfunction in human trisomies.Altered intrinsic and network properties of neocortical neurons in the Ts65Dn mouse model of Down syndromeAnalysis of adult cerebral cortex and hippocampus transcriptomes reveals unique molecular changes in the Ts1Cje mouse model of down syndrome.The physiological role of the amyloid precursor protein as an adhesion molecule in the developing nervous system.DYRK1A-mediated Cyclin D1 Degradation in Neural Stem Cells Contributes to the Neurogenic Cortical Defects in Down Syndrome.
P2860
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P2860
description
2011 nî lūn-bûn
@nan
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
2011年论文
@zh
2011年论文
@zh-cn
name
Trisomy 21 and early brain development
@ast
Trisomy 21 and early brain development
@en
type
label
Trisomy 21 and early brain development
@ast
Trisomy 21 and early brain development
@en
prefLabel
Trisomy 21 and early brain development
@ast
Trisomy 21 and early brain development
@en
P2860
P1476
Trisomy 21 and early brain development
@en
P2093
Roger H Reeves
P2860
P356
10.1016/J.TINS.2011.11.001
P577
2011-12-09T00:00:00Z