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Enhanced GIRK2 channel signaling in Down syndrome: A feasible role in the development of abnormal nascent neural circuits

Frontiers in genetics, 2022-09, Vol.13, p.1006068-1006068

Kleschevnikov, Alexander M

2022

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Down Syndrome Cognitive Phenotypes Modeled in Mice Trisomic for All HSA 21 Homologues

PloS one, 2015-07, Vol.10 (7), p.e0134861-e0134861

2015

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Monoacylglycerol lipase inhibitor JZL184 improves behavior and neural properties in Ts65Dn mice, a model of down syndrome

PloS one, 2014-12, Vol.9 (12), p.e114521

2014

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Genetic dissection of the Down syndrome critical region

Human molecular genetics, 2015-11, Vol.24 (22), p.6540-6551

2015

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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

The Journal of neuroscience, 2009-05, Vol.29 (18), p.5938-5948

2009

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Developmental excitatory-to-inhibitory GABA polarity switch is delayed in Ts65Dn mice, a genetic model of Down syndrome

Neurobiology of disease, 2018-07, Vol.115, p.1-8

2018

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Synaptic and cognitive abnormalities in mouse models of down syndrome: Exploring genotype-phenotype relationships

Journal of comparative neurology (1911), 2007-10, Vol.504 (4), p.329-345

2007

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Evidence that increased Kcnj6 gene dose is necessary for deficits in behavior and dentate gyrus synaptic plasticity in the Ts65Dn mouse model of Down syndrome

Neurobiology of disease, 2017-07, Vol.103, p.1-10

2017

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Hippocampal Long-Term Potentiation Suppressed by Increased Inhibition in the Ts65Dn Mouse, a Genetic Model of Down Syndrome

The Journal of neuroscience, 2004-09, Vol.24 (37), p.8153-8160

2004

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Increased efficiency of the GABAA and GABAB receptor-mediated neurotransmission in the Ts65Dn mouse model of Down syndrome

Neurobiology of disease, 2012-02, Vol.45 (2), p.683-691

2012

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Increased App Expression in a Mouse Model of Down's Syndrome Disrupts NGF Transport and Causes Cholinergic Neuron Degeneration

Neuron (Cambridge, Mass.), 2006-07, Vol.51 (1), p.29-42

2006

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Traumatic brain injury enhances neuroinflammation and lesion volume in caveolin deficient mice

Journal of neuroinflammation, 2014-03, Vol.11 (1), p.39-39, Article 39

2014

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An Anti-β-Amyloid Vaccine for Treating Cognitive Deficits in a Mouse Model of Down Syndrome

PloS one, 2016-03, Vol.11 (3), p.e0152471-e0152471

2016

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Three-dimensional synaptic ultrastructure in the dentate gyrus and hippocampal area CA3 in the Ts65Dn mouse model of down syndrome

Journal of comparative neurology (1911), 2011-05, Vol.519 (7), p.1338-1354

2011

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Mouse Models for Down Syndrome-Associated Developmental Cognitive Disabilities

Developmental neuroscience, 2011-01, Vol.33 (5), p.404-413

2011

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Targeting increased levels of APP in Down syndrome: Posiphen‐mediated reductions in APP and its products reverse endosomal phenotypes in the Ts65Dn mouse model

Alzheimer's & dementia, 2021-02, Vol.17 (2), p.271-292

2021

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Down syndrome

Handbook of Clinical Neurology, 2019, Vol.167, p.321-336

2019

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Neuron-Targeted Caveolin-1 Promotes Ultrastructural and Functional Hippocampal Synaptic Plasticity

Cerebral cortex (New York, N.Y. 1991), 2018-09, Vol.28 (9), p.3255-3266

2018

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Acute neuroinflammation provokes intracellular acidification in mouse hippocampus

Journal of neuroinflammation, 2016-11, Vol.13 (1), p.283-283, Article 283

2016

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Excitatory-inhibitory relationship in the fascia dentata in the Ts65Dn mouse model of down syndrome

Journal of comparative neurology (1911), 2009-02, Vol.512 (4), p.453-466

2009

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Synaptic structural abnormalities in the Ts65Dn mouse model of down syndrome

Journal of comparative neurology (1911), 2004-12, Vol.480 (3), p.281-298

2004

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Human chromosome 21 orthologous region on mouse chromosome 17 is a major determinant of Down syndrome-related developmental cognitive deficits

Human molecular genetics, 2014-02, Vol.23 (3), p.578-589

2014

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Long-term potentiation recruits a trisynaptic excitatory associative network within the mouse dentate gyrus

The European journal of neuroscience, 2003-06, Vol.17 (12), p.2690-2702

2003

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Genetic analysis of Down syndrome facilitated by mouse chromosome engineering

Bioengineered, 2012-01, Vol.3 (1), p.8-12

2012

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Deficits in cognition and synaptic plasticity in a mouse model of Down syndrome ameliorated by GABAB receptor antagonists

The Journal of neuroscience, 2012-07, Vol.32 (27), p.9217-9227

2012

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Enhanced GIRK2 channel signaling in Down syndrome: A feasible role in the development of abnormal nascent neural circuits

Down Syndrome Cognitive Phenotypes Modeled in Mice Trisomic for All HSA 21 Homologues

Monoacylglycerol lipase inhibitor JZL184 improves behavior and neural properties in Ts65Dn mice, a model of down syndrome

Genetic dissection of the Down syndrome critical region

The "Down Syndrome Critical Region" Is Sufficient in the Mouse Model to Confer Behavioral, Neurophysiological, and Synaptic Phenotypes Characteristic of Down Syndrome

Developmental excitatory-to-inhibitory GABA polarity switch is delayed in Ts65Dn mice, a genetic model of Down syndrome

Synaptic and cognitive abnormalities in mouse models of down syndrome: Exploring genotype-phenotype relationships

Evidence that increased Kcnj6 gene dose is necessary for deficits in behavior and dentate gyrus synaptic plasticity in the Ts65Dn mouse model of Down syndrome

Hippocampal Long-Term Potentiation Suppressed by Increased Inhibition in the Ts65Dn Mouse, a Genetic Model of Down Syndrome

Increased efficiency of the GABAA and GABAB receptor-mediated neurotransmission in the Ts65Dn mouse model of Down syndrome

Increased App Expression in a Mouse Model of Down's Syndrome Disrupts NGF Transport and Causes Cholinergic Neuron Degeneration

Traumatic brain injury enhances neuroinflammation and lesion volume in caveolin deficient mice

An Anti-β-Amyloid Vaccine for Treating Cognitive Deficits in a Mouse Model of Down Syndrome

Three-dimensional synaptic ultrastructure in the dentate gyrus and hippocampal area CA3 in the Ts65Dn mouse model of down syndrome

Mouse Models for Down Syndrome-Associated Developmental Cognitive Disabilities

Targeting increased levels of APP in Down syndrome: Posiphen‐mediated reductions in APP and its products reverse endosomal phenotypes in the Ts65Dn mouse model

Down syndrome

Neuron-Targeted Caveolin-1 Promotes Ultrastructural and Functional Hippocampal Synaptic Plasticity

Acute neuroinflammation provokes intracellular acidification in mouse hippocampus

Excitatory-inhibitory relationship in the fascia dentata in the Ts65Dn mouse model of down syndrome

Synaptic structural abnormalities in the Ts65Dn mouse model of down syndrome

Human chromosome 21 orthologous region on mouse chromosome 17 is a major determinant of Down syndrome-related developmental cognitive deficits

Long-term potentiation recruits a trisynaptic excitatory associative network within the mouse dentate gyrus

Genetic analysis of Down syndrome facilitated by mouse chromosome engineering

Deficits in cognition and synaptic plasticity in a mouse model of Down syndrome ameliorated by GABAB receptor antagonists

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