Olig1 and Olig2 triplication causes developmental brain defects in Down syndrome - Wikidata - awgldk - TriplyDB

Olig1 and Olig2 triplication causes developmental brain defects in Down syndrome

Olig1 and Olig2 triplication causes developmental brain defects in Down syndrome

http://www.wikidata.org/entity/Q28288207

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Down syndrome: searching for the genetic culprits Dishing out mini-brains: Current progress and future prospects in brain organoid research A new look at an old drug: neuroprotective effects and therapeutic potentials of lithium salts Timing of therapies for Down syndrome: the sooner, the better Mouse models of Down syndrome as a tool to unravel the causes of mental disabilities Down Syndrome: Current Status, Challenges and Future Perspectives GABAA receptor subtypes: Therapeutic potential in Down syndrome, affective disorders, schizophrenia, and autism.Investigating mechanisms underlying neurodevelopmental phenotypes of autistic and intellectual disability disorders: a perspective.Brain plasticity and disease: a matter of inhibition.Effects of individual segmental trisomies of human chromosome 21 syntenic regions on hippocampal long-term potentiation and cognitive behaviors in mice.Strategies for analyzing neuronal progenitor development and neuronal migration in the developing cerebral cortex.Lithium rescues synaptic plasticity and memory in Down syndrome mice.Multiplex genetic fate mapping reveals a novel route of neocortical neurogenesis, which is altered in the Ts65Dn mouse model of Down syndrome Modulation of GABAergic transmission in development and neurodevelopmental disorders: investigating physiology and pathology to gain therapeutic perspectives.A systematic enhancer screen using lentivector transgenesis identifies conserved and non-conserved functional elements at the Olig1 and Olig2 locus.Enhanced derivation of human pluripotent stem cell-derived cortical glutamatergic neurons by a small molecule.Developmentally altered inhibition in Ts65Dn, a mouse model of Down syndrome Dysfunctional hippocampal inhibition in the Ts65Dn mouse model of Down syndrome.Deficits in human trisomy 21 iPSCs and neurons.Negative regulation of miRNA-9 on oligodendrocyte lineage gene 1 during hypoxic-ischemic brain damage.Overexpression of Dyrk1A is implicated in several cognitive, electrophysiological and neuromorphological alterations found in a mouse model of Down syndrome Abnormal microRNA expression in Ts65Dn hippocampus and whole blood: contributions to Down syndrome phenotypes.Global DNA hypermethylation in down syndrome placenta Selective impact of MeCP2 and associated histone deacetylases on the dynamics of evoked excitatory neurotransmission Chronic P7C3 treatment restores hippocampal neurogenesis in the Ts65Dn mouse model of Down Syndrome [Corrected].Galantamine improves olfactory learning in the Ts65Dn mouse model of Down syndrome.Disruption of neurogenesis and cortical development in transgenic mice misexpressing Olig2, a gene in the Down syndrome critical region Amygdala regulation of fear and emotionality in fragile X syndrome.Mouse models for Down syndrome-associated developmental cognitive disabilities Environmental enrichment rescues postnatal neurogenesis defect in the male and female Ts65Dn mouse model of Down syndrome.Increased efficiency of the GABAA and GABAB receptor-mediated neurotransmission in the Ts65Dn mouse model of Down syndrome Deletion of the App-Runx1 region in mice models human partial monosomy 21.Trisomy 21 and early brain development OLIG2 over-expression impairs proliferation of human Down syndrome neural progenitors.Molecular and cellular alterations in Down syndrome: toward the identification of targets for therapeutics From 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.Genetic dissection of Down syndrome-associated congenital heart defects using a new mouse mapping panel.Absence 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.

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Olig1 and Olig2 triplication causes developmental brain defects in Down syndrome

http://www.wikidata.org/entity/Q28288207

description

2010 nî lūn-bûn

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2010 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի օգոստոսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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name

Olig1 and Olig2 triplication causes developmental brain defects in Down syndrome

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Olig1 and Olig2 triplication causes developmental brain defects in Down syndrome

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Olig1 and Olig2 triplication causes developmental brain defects in Down syndrome

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Olig1 and Olig2 triplication causes developmental brain defects in Down syndrome

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Olig1 and Olig2 triplication causes developmental brain defects in Down syndrome

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Olig1 and Olig2 triplication causes developmental brain defects in Down syndrome

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Olig1 and Olig2 triplication causes developmental brain defects in Down syndrome

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Olig1 and Olig2 triplication causes developmental brain defects in Down syndrome

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Olig1 and Olig2 triplication causes developmental brain defects in Down syndrome

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Nature Neuroscience

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Olig1 and Olig2 triplication causes developmental brain defects in Down syndrome

@en

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John T R Isaac

http://www.w3.org/2001/XMLSchema#string

Lina Chakrabarti

http://www.w3.org/2001/XMLSchema#string

Rosalind S E Carney

http://www.w3.org/2001/XMLSchema#string

Tyler K Best

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Zygmunt Galdzicki

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P2860

DLX-1, DLX-2, and DLX-5 expression define distinct stages of basal forebrain differentiation

Lhx6 activity is required for the normal migration and specification of cortical interneuron subtypes

Loss of Nkx2.1 homeobox gene function results in a ventral to dorsal molecular respecification within the basal telencephalon: evidence for a transformation of the pallidum into the striatum

Common developmental requirement for Olig function indicates a motor neuron/oligodendrocyte connection

Interneurons of the neocortical inhibitory system

Proneural genes and the specification of neural cell types

Interneurons of the hippocampus

The origin and specification of cortical interneurons

Advanced microscopic imaging methods to investigate cortical development and the etiology of mental retardation.

Fetal life in Down syndrome starts with normal neuronal density but impaired dendritic spines and synaptosomal structure.

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10.1038/NN.2600

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8

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13

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Nathan P Cramer

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2010-07-18T00:00:00Z

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45272232

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20639873

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