NO synthase 2 (NOS2) deletion promotes multiple pathologies in a mouse model of Alzheimer's disease. - Wikidata - wikimedia - TriplyDB

NO synthase 2 (NOS2) deletion promotes multiple pathologies in a mouse model of Alzheimer's disease.

NO synthase 2 (NOS2) deletion promotes multiple pathologies in a mouse model of Alzheimer's disease.

http://www.wikidata.org/entity/Q34998995

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Behavioral assays with mouse models of Alzheimer's disease: practical considerations and guidelines.Enhanced astrocytic nitric oxide production and neuronal modifications in the neocortex of a NOS2 mutant mouse An NO donor approach to neuroprotective and procognitive estrogen therapy overcomes loss of NO synthase function and potentially thrombotic risk Aberrant protein S-nitrosylation contributes to the pathophysiology of neurodegenerative diseases Berberine chloride can ameliorate the spatial memory impairment and increase the expression of interleukin-1beta and inducible nitric oxide synthase in the rat model of Alzheimer's disease Potential mechanisms linking cholesterol to Alzheimer's disease-like pathology in rabbit brain, hippocampal organotypic slices, and skeletal muscle The SPRY domain-containing SOCS box protein SPSB2 targets iNOS for proteasomal degradation.mNos2 deletion and human NOS2 replacement in Alzheimer disease models Accelerating drug discovery for Alzheimer's disease: best practices for preclinical animal studies Angiotensin-converting enzyme insertion/deletion polymorphism is not a major determining factor in the development of sporadic Alzheimer disease: evidence from an updated meta-analysis Neuroprotective strategies involving ROS in Alzheimer disease.Activation of matrix metalloproteinases following anti-Aβ immunotherapy; implications for microhemorrhage occurrence.Atg7 enhances host defense against infection via downregulation of superoxide but upregulation of nitric oxide Diverse inflammatory responses in transgenic mouse models of Alzheimer's disease and the effect of immunotherapy on these responses.The classification of microglial activation phenotypes on neurodegeneration and regeneration in Alzheimer's disease brain.Neuronal c-Abl overexpression leads to neuronal loss and neuroinflammation in the mouse forebrain.Metabotropic glutamate receptors inhibit microglial glutamate release.Quantitative measurement of postural sway in mouse models of human neurodegenerative disease In vivo hippocampal microdialysis reveals impairment of NMDA receptor-cGMP signaling in APP(SW) and APP(SW)/PS1(L166P) Alzheimer's transgenic mice Anti-amyloid-beta immunotherapy in Alzheimer's disease: relevance of transgenic mouse studies to clinical trials.Vascular amyloid alters astrocytic water and potassium channels in mouse models and humans with Alzheimer's disease Absence of Nitric Oxide Synthase 3 Increases Amyloid β-Protein Pathology in Tg-5xFAD Mice.Cannabinoid regulation of nitric oxide synthase I (nNOS) in neuronal cells Alzheimer's disease: cerebrovascular dysfunction, oxidative stress, and advanced clinical therapies The effects of NOS2 gene deletion on mice expressing mutated human AbetaPP.Longitudinal study of differential protein expression in an Alzheimer's mouse model lacking inducible nitric oxide synthase.Nitric Oxide: Exploring the Contextual Link with Alzheimer's Disease Heterogeneity of microglial activation in the innate immune response in the brain.Antioxidant gene therapy against neuronal cell death.Immunotherapeutic approaches for Alzheimer's disease in transgenic mouse models.Murine models of Alzheimer's disease and their use in developing immunotherapies.Reactive astrocytes as therapeutic targets for CNS disorders.Mitochondrial dysfunction--a pharmacological target in Alzheimer's disease.Modulation of inflammation in transgenic models of Alzheimer's disease Berberine Decreased Inducible Nitric Oxide Synthase mRNA Stability through Negative Regulation of Human Antigen R in Lipopolysaccharide-Induced Macrophages.Emerging pathways driving early synaptic pathology in Alzheimer's disease.Nitric oxide signaling is recruited as a compensatory mechanism for sustaining synaptic plasticity in Alzheimer's disease mice.Amyloid reduction by amyloid-beta vaccination also reduces mouse tau pathology and protects from neuron loss in two mouse models of Alzheimer's disease.Oxidative stress mediates tau-induced neurodegeneration in Drosophila Correlated inflammatory responses and neurodegeneration in peptide-injected animal models of Alzheimer's disease.

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P2860

NO synthase 2 (NOS2) deletion promotes multiple pathologies in a mouse model of Alzheimer's disease.

http://www.wikidata.org/entity/Q34998995

description

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2006 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

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NO synthase 2 (NOS2) deletion ...... model of Alzheimer's disease.

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NO synthase 2 (NOS2) deletion ...... model of Alzheimer's disease.

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NO synthase 2

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NO synthase 2 (NOS2) deletion ...... model of Alzheimer's disease.

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NO synthase 2 (NOS2) deletion ...... model of Alzheimer's disease.

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NO synthase 2 (NOS2) deletion ...... model of Alzheimer's disease.

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NO synthase 2 (NOS2) deletion ...... model of Alzheimer's disease.

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C A Colton

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D A Wink

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H Dawson

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P2860

Correlative Memory Deficits, Abeta Elevation, and Amyloid Plaques in Transgenic Mice

Tau pathology in Alzheimer disease and other tauopathies

Caspase cleavage of tau: linking amyloid and neurofibrillary tangles in Alzheimer's disease

Thrombospondin-1 inhibits endothelial cell responses to nitric oxide in a cGMP-dependent manner

The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics

Aberrant expression of nitric oxide synthase III in Alzheimer's disease: relevance to cerebral vasculopathy and neurodegeneration

Triple-transgenic model of Alzheimer's disease with plaques and tangles: intracellular Abeta and synaptic dysfunction

Resident microglia from adult mice are refractory to nitric oxide-inducing stimuli due to impaired NOS2 gene expression.

S-Nitrosylation of mitochondrial caspases

Caspase-cleavage of tau is an early event in Alzheimer disease tangle pathology

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