Complement component C3 and complement receptor type 3 contribute to the phagocytosis and clearance of fibrillar Aβ by microglia - Wikidata - awgldk - TriplyDB

Complement component C3 and complement receptor type 3 contribute to the phagocytosis and clearance of fibrillar Aβ by microglia

Complement component C3 and complement receptor type 3 contribute to the phagocytosis and clearance of fibrillar Aβ by microglia

http://www.wikidata.org/entity/Q30665205

about

Galactic cosmic radiation leads to cognitive impairment and increased aβ plaque accumulation in a mouse model of Alzheimer's disease Mechanisms of Aβ Clearance and Degradation by Glial Cells Towards understanding the roles of heparan sulfate proteoglycans in Alzheimer's disease Microglia communication: Parallels between aging and Alzheimer's disease Exploring Biomarkers for Alzheimer's Disease Amyloid fibrils composed of hexameric peptides attenuate neuroinflammation.Reactomes of porcine alveolar macrophages infected with porcine reproductive and respiratory syndrome virus.Activation of the nuclear receptor PPARδ is neuroprotective in a transgenic mouse model of Alzheimer's disease through inhibition of inflammation Role of α-synuclein in inducing innate and adaptive immunity in Parkinson disease.Nuclear receptors license phagocytosis by trem2+ myeloid cells in mouse models of Alzheimer's disease.Ablation of CCAAT/Enhancer-Binding Protein Delta (C/EBPD): Increased Plaque Burden in a Murine Alzheimer's Disease Model Active immunization against complement factor C5a: a new therapeutic approach for Alzheimer's disease Telmisartan Modulates Glial Activation: In Vitro and In Vivo Studies Forebrain microglia from wild-type but not adult 5xFAD mice prevent amyloid-β plaque formation in organotypic hippocampal slice cultures.A comparative review of cell culture systems for the study of microglial biology in Alzheimer's disease.Astrocyte-Microglia Cross Talk through Complement Activation Modulates Amyloid Pathology in Mouse Models of Alzheimer's Disease.Signaling pathways regulating neuron-glia interaction and their implications in Alzheimer's disease.Sustained interleukin-1β overexpression exacerbates tau pathology despite reduced amyloid burden in an Alzheimer's mouse model.Electroacupuncture Promotes Remyelination after Cuprizone Treatment by Enhancing Myelin Debris Clearance.Tau passive immunization inhibits not only tau but also Aβ pathology Ganglioside deficiency causes inflammation and neurodegeneration via the activation of complement system in the spinal cord.Microglial activatory (immunoreceptor tyrosine-based activation motif)- and inhibitory (immunoreceptor tyrosine-based inhibition motif)-signaling receptors for recognition of the neuronal glycocalyx.Microglia receptors and their implications in the response to amyloid β for Alzheimer's disease pathogenesis.Amyloid β-Induced Redistribution of Transcriptional Factor EB and Lysosomal Dysfunction in Primary Microglial Cells.Protein aggregates stimulate macropinocytosis facilitating their propagation IgM-Dependent Phagocytosis in Microglia Is Mediated by Complement Receptor 3, Not Fcα/μ Receptor.Periodontal and other oral manifestations of immunodeficiency diseases.Prelysosomal Compartments in the Unconventional Secretion of Amyloidogenic Seeds.Complement regulation and kidney diseases: recent knowledge of the double-edged roles of complement activation in nephrology.Extracellular aggregated Cu/Zn superoxide dismutase activates microglia to give a cytotoxic phenotype.Amyloid-β42 protofibrils are internalized by microglia more extensively than monomers.The gamma chain subunit of Fc receptors is required for alpha-synuclein-induced pro-inflammatory signaling in microglia.Microglial complement receptor 3 regulates brain Aβ levels through secreted proteolytic activity.Microglia, Alzheimer's disease, and complement.Pharmacological Tools to Activate Microglia and their Possible use to Study Neural Network Patho-physiology.Tau passive immunization blocks seeding and spread of Alzheimer hyperphosphorylated Tau-induced pathology in 3 × Tg-AD mice.Complement C3 deficiency protects against neurodegeneration in aged plaque-rich APP/PS1 mice.Angiotensin Converting Enzyme Inhibitors Ameliorate Brain Inflammation Associated with Microglial Activation: Possible Implications for Alzheimer's Disease.Transcriptome analysis of alcohol-treated microglia reveals downregulation of beta amyloid phagocytosis.A preclinical perspective on the enhanced vulnerability to Alzheimer's disease after early-life stress.

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P2860

Complement component C3 and complement receptor type 3 contribute to the phagocytosis and clearance of fibrillar Aβ by microglia

http://www.wikidata.org/entity/Q30665205

description

2012 nî lūn-bûn

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2012 թուականի Մարտին հրատարակուած գիտական յօդուած

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2012 թվականի մարտին հրատարակված գիտական հոդված

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2012年の論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年论文

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name

Complement component C3 and co ...... e of fibrillar Aβ by microglia

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Complement component C3 and co ...... e of fibrillar Aβ by microglia

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Complement component C3 and co ...... e of fibrillar Aβ by microglia

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Complement component C3 and co ...... e of fibrillar Aβ by microglia

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Complement component C3 and co ...... e of fibrillar Aβ by microglia

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Complement component C3 and co ...... e of fibrillar Aβ by microglia

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Complement component C3 and co ...... e of fibrillar Aβ by microglia

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P2093

Beth Ostaszewski

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

Bin Liu

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

Cynthia A Lemere

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

Ganesh M Shankar

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

Hongjun Fu

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

Isabel M Costantino

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

Jeffrey L Frost

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

Michael C Carroll

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

Ming Jin

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

Soyon Hong

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

P2860

RAGE and amyloid-beta peptide neurotoxicity in Alzheimer's disease

Amyloid-beta protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory

Complement receptor 3 (CD11b/CD18) is implicated in the elimination of β-amyloid peptides.

Studies of group B streptococcal infection in mice deficient in complement component C3 or C4 demonstrate an essential role for complement in both innate and acquired immunity.

Prominent neurodegeneration and increased plaque formation in complement-inhibited Alzheimer's mice.

Microglial MAC1 receptor and PI3K are essential in mediating β-amyloid peptide-induced microglial activation and subsequent neurotoxicity

Activation of complement in the central nervous system: roles in neurodegeneration and neuroprotection.

Activation of microglia acidifies lysosomes and leads to degradation of Alzheimer amyloid fibrils.

CD36, a class B scavenger receptor, is expressed on microglia in Alzheimer's disease brains and can mediate production of reactive oxygen species in response to beta-amyloid fibrils.

A protective role for innate immunity in systemic lupus erythematosus.

P304

993-1003

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scholarly article

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10.1002/GLIA.22331

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6

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60

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2012-03-21T00:00:00Z

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221966991

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22438044

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

P921

Complement component 3

Integrin alpha-M

Macrophage scavenger receptor 1

P932

3325361

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