Blocking TGF-beta-Smad2/3 innate immune signaling mitigates Alzheimer-like pathology. - Wikidata - awgldk - TriplyDB

Blocking TGF-beta-Smad2/3 innate immune signaling mitigates Alzheimer-like pathology.

Blocking TGF-beta-Smad2/3 innate immune signaling mitigates Alzheimer-like pathology.

http://www.wikidata.org/entity/Q37113528

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Anti-inflammatory and pro-inflammatory roles of TGF-beta, IL-10, and IL-22 in immunity and autoimmunity Neural stem/progenitor cells in Alzheimer's disease Targeting innate immunity for neurodegenerative disorders of the central nervous system Imaging of Leukocyte Trafficking in Alzheimer's Disease Myeloid Dendritic Cells are Potential Players in Human Neurodegenerative Diseases The role of the immune system in neurodegenerative disorders: Adaptive or maladaptive?How do immune cells support and shape the brain in health, disease, and aging?Neuroinflammation in Alzheimer's disease Innate immunity in Alzheimer's disease: a complex affair Neuroimmunological processes in Parkinson's disease and their relation to α-synuclein: microglia as the referee between neuronal processes and peripheral immunity Chemical dampening of Ly6C(hi) monocytes in the periphery produces anti-depressant effects in mice.Oral TNFα Modulation Alters Neutrophil Infiltration, Improves Cognition and Diminishes Tau and Amyloid Pathology in the 3xTgAD Mouse Model CCL2 accelerates microglia-mediated Abeta oligomer formation and progression of neurocognitive dysfunction Toll-like Receptor 7 Mitigates Lethal West Nile Encephalitis via Interleukin 23-Dependent Immune Cell Infiltration and Homing Checkpoints to the Brain: Directing Myeloid Cell Migration to the Central Nervous System Innate Immunity Fights Alzheimer's Disease Neuroinflammation in Alzheimer's disease Mechanisms of mononuclear phagocyte recruitment in Alzheimer's disease Interactions between inflammation, sex steroids, and Alzheimer's disease risk factors Ferulic acid is a nutraceutical β-secretase modulator that improves behavioral impairment and alzheimer-like pathology in transgenic mice Network Topology Analysis of Post-Mortem Brain Microarrays Identifies More Alzheimer's Related Genes and MicroRNAs and Points to Novel Routes for Fighting with the Disease TGF-beta1 blockade of microglial chemotaxis toward Abeta aggregates involves SMAD signaling and down-regulation of CCL5 Early growth response 1 (Egr-1) regulates phosphorylation of microtubule-associated protein tau in mammalian brain Microglia demonstrate age-dependent interaction with amyloid-β fibrils Reduction of oxidative stress, amyloid deposition, and memory deficit by manganese superoxide dismutase overexpression in a transgenic mouse model of Alzheimer's disease.Role of the macrophage inflammatory protein-1alpha/CC chemokine receptor 5 signaling pathway in the neuroinflammatory response and cognitive deficits induced by beta-amyloid peptide TGF-β induces TIAF1 self-aggregation via type II receptor-independent signaling that leads to generation of amyloid β plaques in Alzheimer's disease.Intact memory in TGF-β1 transgenic mice featuring chronic cerebrovascular deficit: recovery with pioglitazone Triterpenoid CDDO-methylamide improves memory and decreases amyloid plaques in a transgenic mouse model of Alzheimer's disease.Microglial beclin 1 regulates retromer trafficking and phagocytosis and is impaired in Alzheimer's disease.HIF-1α is a protective factor in conditional PHD2-deficient mice suffering from severe HIF-2α-induced excessive erythropoiesis.A new mesenchymal stem cell (MSC) paradigm: polarization into a pro-inflammatory MSC1 or an Immunosuppressive MSC2 phenotype.HIV-1 stimulates nuclear entry of amyloid beta via dynamin dependent EEA1 and TGF-β/Smad signaling.Inflammation, microglia, and Alzheimer's disease.Can peripheral leukocytes be used as Alzheimer's disease biomarkers?YXQN Reduces Alzheimer's Disease-Like Pathology and Cognitive Decline in APPswePS1dE9 Transgenic Mice.Overcoming the hurdles in using mouse genetic models that block TGF-beta signaling.Intestinal microbial dysbiosis aggravates the progression of Alzheimer's disease in Drosophila Mutant presenilin-1 deregulated peripheral immunity exacerbates Alzheimer-like pathology Interleukin-1β mediated amyloid plaque clearance is independent of CCR2 signaling in the APP/PS1 mouse model of Alzheimer's disease.

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Blocking TGF-beta-Smad2/3 innate immune signaling mitigates Alzheimer-like pathology.

http://www.wikidata.org/entity/Q37113528

description

article científic

@ca

article scientifique

@fr

articolo scientifico

@it

artigo científico

@pt

bilimsel makale

@tr

scientific article published on June 2008

@en

vedecký článok

@sk

vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

Blocking TGF-beta-Smad2/3 innate immune signaling mitigates Alzheimer-like pathology.

@en

Blocking TGF-beta-Smad2/3 innate immune signaling mitigates Alzheimer-like pathology.

@nl

type

label

Blocking TGF-beta-Smad2/3 innate immune signaling mitigates Alzheimer-like pathology.

@en

Blocking TGF-beta-Smad2/3 innate immune signaling mitigates Alzheimer-like pathology.

@nl

prefLabel

Blocking TGF-beta-Smad2/3 innate immune signaling mitigates Alzheimer-like pathology.

@en

Blocking TGF-beta-Smad2/3 innate immune signaling mitigates Alzheimer-like pathology.

@nl

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Nature Medicine

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Blocking TGF-beta-Smad2/3 innate immune signaling mitigates Alzheimer-like pathology.

@en

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Christine A Szekely

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

Jun Tan

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

Richard A Flavell

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

Ronald S Duman

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

Takashi Mori

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

Terrence Town

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

Yasmina Laouar

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

P2860

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

The microglial "activation" continuum: from innate to adaptive responses

Alzheimer's disease: genes, proteins, and therapy

Inflammation and Alzheimer's disease

Transforming growth factor-beta regulation of immune responses

Blood monocytes consist of two principal subsets with distinct migratory properties

The relationship between Abeta and memory in the Tg2576 mouse model of Alzheimer's disease.

Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes.

Deficiency in neuronal TGF-beta signaling promotes neurodegeneration and Alzheimer's pathology

Augmented senile plaque load in aged female beta-amyloid precursor protein-transgenic mice

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681-687

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scholarly article

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10.1038/NM1781

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P407

P433

6

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P478

14

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Christopher Pittenger

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2008-06-01T00:00:00Z

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5331361

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18516051

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Alzheimer's disease

P932

2649699

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