C3-dependent mechanism of microglial priming relevant to multiple sclerosis. - Wikidata - awgldk - TriplyDB

C3-dependent mechanism of microglial priming relevant to multiple sclerosis.

C3-dependent mechanism of microglial priming relevant to multiple sclerosis.

http://www.wikidata.org/entity/Q35734866

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From development to dysfunction: microglia and the complement cascade in CNS homeostasis Role of microglia in CNS autoimmunity Ovariectomy and subsequent treatment with estrogen receptor agonists tune the innate immune system of the hippocampus in middle-aged female rats Complement activation in multiple sclerosis plaques: an immunohistochemical analysis.Enhanced uptake of multiple sclerosis-derived myelin by THP-1 macrophages and primary human microglia.The role of microglia in human disease: therapeutic tool or target?Microglial phenotype and adaptation.Selective upregulation of scavenger receptors in and around demyelinating areas in multiple sclerosis.Cardioembolic and small vessel disease stroke show differences in associations between systemic C3 levels and outcome Complement component C3 and butyrylcholinesterase activity are associated with neurodegeneration and clinical disability in multiple sclerosis.Clinical and genetic factors associated with progression of geographic atrophy lesions in age-related macular degeneration Involvement of calcitonin gene-related peptide and receptor component protein in experimental autoimmune encephalomyelitis.The evolving landscape of neurotoxicity by unconjugated bilirubin: role of glial cells and inflammation.Mast Cells are Important Modifiers of Autoimmune Disease: With so Much Evidence, Why is There Still Controversy?Blood coagulation protein fibrinogen promotes autoimmunity and demyelination via chemokine release and antigen presentation Complement receptor 2 is up regulated in the spinal cord following nerve root injury and modulates the spinal cord response.A postnatal peak in microglial development in the mouse hippocampus is correlated with heightened sensitivity to seizure triggers.Complement component C3a plays a critical role in endothelial activation and leukocyte recruitment into the brain Menopause leads to elevated expression of macrophage-associated genes in the aging frontal cortex: rat and human studies identify strikingly similar changes.Acute phase proteins are major clients for the chaperone action of α₂-macroglobulin in human plasma A shift in microglial β-amyloid binding in Alzheimer's disease is associated with cerebral amyloid angiopathy.Hippocampal Neuroinflammation, Functional Connectivity, and Depressive Symptoms in Multiple Sclerosis.Prior Binge Ethanol Exposure Potentiates the Microglial Response in a Model of Alcohol-Induced Neurodegeneration.Complement component 3 (C3) expression in the hippocampus after excitotoxic injury: role of C/EBPβ.Myelinosome formation represents an early stage of oligodendrocyte damage in multiple sclerosis and its animal model.Complement C3 on microglial clusters in multiple sclerosis occur in chronic but not acute disease: Implication for disease pathogenesis.Electroacupuncture Promotes Remyelination after Cuprizone Treatment by Enhancing Myelin Debris Clearance.The nucleotide-binding leucine-rich repeat (NLR) family member NLRX1 mediates protection against experimental autoimmune encephalomyelitis and represses macrophage/microglia-induced inflammation.Microglia and neurodegeneration: the role of systemic inflammation.Complement activation in the injured central nervous system: another dual-edged sword?Innate immunity and neuroinflammation.Mechanisms of white matter damage in multiple sclerosis.Macrophage subsets and microglia in multiple sclerosis.The role of complement in neurological and neuropsychiatric diseases.Regulator-dependent mechanisms of C3b processing by factor I allow differentiation of immune responses.Tissue microarray methodology identifies complement pathway activation and dysregulation in progressive multiple sclerosis.Dietary n-3 PUFAs Deficiency Increases Vulnerability to Inflammation-Induced Spatial Memory Impairment.Activation status of human microglia is dependent on lesion formation stage and remyelination in multiple sclerosis.Deletion of Crry, the murine ortholog of the sporadic Alzheimer's disease risk gene CR1, impacts tau phosphorylation and brain CFH.Microglia, Alzheimer's disease, and complement.

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P2860

C3-dependent mechanism of microglial priming relevant to multiple sclerosis.

http://www.wikidata.org/entity/Q35734866

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name

C3-dependent mechanism of microglial priming relevant to multiple sclerosis.

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C3-dependent mechanism of microglial priming relevant to multiple sclerosis.

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type

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C3-dependent mechanism of microglial priming relevant to multiple sclerosis.

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C3-dependent mechanism of microglial priming relevant to multiple sclerosis.

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C3-dependent mechanism of microglial priming relevant to multiple sclerosis.

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C3-dependent mechanism of microglial priming relevant to multiple sclerosis.

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Proceedings of the National Academy of Sciences of the United States of America

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C3-dependent mechanism of microglial priming relevant to multiple sclerosis

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P2093

Inge Huitinga

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

James W Neal

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Marieta M Ruseva

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Timothy R Hughes

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Valeria Ramaglia

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Xiaobo Wu

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P2860

Crry deficiency in complement sufficient mice: C3 consumption occurs without associated renal injury

Complement: a key system for immune surveillance and homeostasis

Microglial physiology: unique stimuli, specialized responses

Downregulation of macrophage inhibitory molecules in multiple sclerosis lesions.

Systemic inflammation and disease progression in Alzheimer disease.

Inflammatory processes induce beta-amyloid precursor protein changes in mouse brain.

Immunoglobulins and complement in postmortem multiple sclerosis tissue.

Systemic infection, interleukin 1beta, and cognitive decline in Alzheimer's disease.

Mouse complement regulatory protein Crry/p65 uses the specific mechanisms of both human decay-accelerating factor and membrane cofactor protein

Transient middle cerebral artery occlusion induces microglial priming in the lumbar spinal cord: a novel model of neuroinflammation

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22219359

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multiple sclerosis

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3271873

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