MyD88 deficiency ameliorates β-amyloidosis in an animal model of Alzheimer's disease - Test2 - elhamkhani - TriplyDB

MyD88 deficiency ameliorates β-amyloidosis in an animal model of Alzheimer's disease

MyD88 deficiency ameliorates β-amyloidosis in an animal model of Alzheimer's disease

http://www.wikidata.org/entity/Q24616286

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Alzheimer's Disease: Mechanism and Approach to Cell Therapy Bioenergetic dysfunction and inflammation in Alzheimer's disease: a possible connection Neuron-released oligomeric α-synuclein is an endogenous agonist of TLR2 for paracrine activation of microglia Retinal dendritic cell recruitment, but not function, was inhibited in MyD88 and TRIF deficient mice.Amyloid-β(1-42) protofibrils stimulate a quantum of secreted IL-1β despite significant intracellular IL-1β accumulation in microglia.MyD88 is dispensable for cerebral amyloidosis and neuroinflammation in APP/PS1 transgenic mice.Inflammasomes as therapeutic targets for Alzheimer's disease.Soluble amyloid triggers a myeloid differentiation factor 88 and interferon regulatory factor 7 dependent neuronal type-1 interferon response in vitro The effects of MyD88 deficiency on exploratory activity, anxiety, motor coordination, and spatial learning in C57BL/6 and APPswe/PS1dE9 mice.Eicosanoid receptor subtype-mediated opposing regulation of TLR-stimulated expression of astrocyte glial-derived neurotrophic factor.Toll-like receptor (TLR) and inflammasome actions in the central nervous system Loss of interleukin receptor-associated kinase 4 signaling suppresses amyloid pathology and alters microglial phenotype in a mouse model of Alzheimer's disease.The neuroendocrine control of the innate immune system in health and brain diseases.Clearance of amyloid-β peptides by microglia and macrophages: the issue of what, when and where.Fractalkine Mediates Communication between Pathogenic Proteins and Microglia: Implications of Anti-Inflammatory Treatments in Different Stages of Neurodegenerative Diseases.Review: experimental manipulations of microglia in mouse models of Alzheimer's pathology: activation reduces amyloid but hastens tau pathology.Modulation of inflammation in transgenic models of Alzheimer's disease Innate immunity in Alzheimer's disease.Compromised MAPK signaling in human diseases: an update.Type-I interferon pathway in neuroinflammation and neurodegeneration: focus on Alzheimer's disease.Reduced photoreceptor death and improved retinal function during retinal degeneration in mice lacking innate immunity adaptor protein MyD88.Intracranial IL-17A overexpression decreases cerebral amyloid angiopathy by upregulation of ABCA1 in an animal model of Alzheimer's disease.Cloning, Characterization, and Expression Analysis of MyD88 in Rana dybowskii.IL-10 alters immunoproteostasis in APP mice, increasing plaque burden and worsening cognitive behavior.Antimalarial drug artemisinin extenuates amyloidogenesis and neuroinflammation in APPswe/PS1dE9 transgenic mice via inhibition of nuclear factor-κB and NLRP3 inflammasome activation.Brain-borne IL-1 adjusts glucoregulation and provides fuel support to astrocytes and neurons in an autocrine/paracrine manner.Microglia in Alzheimer's Disease: A Role for Ion Channels

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MyD88 deficiency ameliorates β-amyloidosis in an animal model of Alzheimer's disease

http://www.wikidata.org/entity/Q24616286

description

2011 nî lūn-bûn

@nan

2011 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի սեպտեմբերին հրատարակված գիտական հոդված

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2011年の論文

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2011年学术文章

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2011年学术文章

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2011年学术文章

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2011年学术文章

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2011年学术文章

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2011年學術文章

@yue

name

MyD88 deficiency ameliorates β-amyloidosis in an animal model of Alzheimer's disease

@ast

MyD88 deficiency ameliorates β-amyloidosis in an animal model of Alzheimer's disease

@en

MyD88 deficiency ameliorates β-amyloidosis in an animal model of Alzheimer's disease

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type

label

MyD88 deficiency ameliorates β-amyloidosis in an animal model of Alzheimer's disease

@ast

MyD88 deficiency ameliorates β-amyloidosis in an animal model of Alzheimer's disease

@en

MyD88 deficiency ameliorates β-amyloidosis in an animal model of Alzheimer's disease

@nl

prefLabel

MyD88 deficiency ameliorates β-amyloidosis in an animal model of Alzheimer's disease

@ast

MyD88 deficiency ameliorates β-amyloidosis in an animal model of Alzheimer's disease

@en

MyD88 deficiency ameliorates β-amyloidosis in an animal model of Alzheimer's disease

@nl

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J.AJPATH.2011.05.045

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The American Journal of Pathology

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MyD88 deficiency ameliorates β-amyloidosis in an animal model of Alzheimer's disease

@en

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Jeong-Eun Lim

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

Jinghong Kou

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

Jingji Jin

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

Ken-ichiro Fukuchi

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

Min Song

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Robert Lalonde

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P2860

Insulin-degrading enzyme regulates extracellular levels of amyloid beta-protein by degradation

CD36 ligands promote sterile inflammation through assembly of a Toll-like receptor 4 and 6 heterodimer

ApoE promotes the proteolytic degradation of Abeta

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

Pattern recognition receptors and inflammation

Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal long-term potentiation in vivo

Inflammation and Alzheimer's disease

Mutant presenilins specifically elevate the levels of the 42 residue beta-amyloid peptide in vivo: evidence for augmentation of a 42-specific gamma secretase

A specific amyloid-beta protein assembly in the brain impairs memory

Diffusible, nonfibrillar ligands derived from Abeta1-42 are potent central nervous system neurotoxins

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Abhinandan Pattanayak

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51496966

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Alzheimer's disease

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