Exacerbation of CNS inflammation and neurodegeneration by systemic LPS treatment is independent of circulating IL-1β and IL-6. - Wikidata - awgldk - TriplyDB

Exacerbation of CNS inflammation and neurodegeneration by systemic LPS treatment is independent of circulating IL-1β and IL-6.

Exacerbation of CNS inflammation and neurodegeneration by systemic LPS treatment is independent of circulating IL-1β and IL-6.

http://www.wikidata.org/entity/Q35057271

about

Intestinal microbiota, probiotics and mental health: from Metchnikoff to modern advances: Part II - contemporary contextual research Overnutrition Determines LPS Regulation of Mycotoxin Induced Neurotoxicity in Neurodegenerative Diseases A novel in vitro model to study pericytes in the neurovascular unit of the developing cortex Stem cell therapy for central nerve system injuries: glial cells hold the key Dexamethasone rescues neurovascular unit integrity from cell damage caused by systemic administration of shiga toxin 2 and lipopolysaccharide in mice motor cortex PKR deficiency alters E. coli-induced sickness behaviors but does not exacerbate neuroimmune responses or bacterial load Impairment of autophagy in the central nervous system during lipopolysaccharide-induced inflammatory stress in mice Phosphorylation and nuclear translocation of integrin β4 induced by a chemical small molecule contribute to apoptosis in vascular endothelial cells.A systematic analysis of the peripheral and CNS effects of systemic LPS, IL-1β, [corrected] TNF-α and IL-6 challenges in C57BL/6 mice Endogenous IL-1 in cognitive function and anxiety: a study in IL-1RI-/- mice General anesthetics inhibit LPS-induced IL-1β expression in glial cells.Systemic inflammation and microglial activation: systematic review of animal experiments The immunology of neurodegeneration.Interdependent and independent roles of type I interferons and IL-6 in innate immune, neuroinflammatory and sickness behaviour responses to systemic poly I:C.Peripheral challenge with a viral mimic upregulates expression of the complement genes in the hippocampus.Magnetic Resonance Spectroscopy discriminates the response to microglial stimulation of wild type and Alzheimer's disease models.Defining the Microglia Response during the Time Course of Chronic Neurodegeneration Euflammation attenuates peripheral inflammation-induced neuroinflammation and mitigates immune-to-brain signaling Inflammation and clinical presentation in neurodegenerative disease: a volatile relationship.Cyclooxygenase-1-dependent prostaglandins mediate susceptibility to systemic inflammation-induced acute cognitive dysfunction.Systemic and localized extra-central nervous system bacterial infections and the risk of dementia among US veterans: A retrospective cohort study.Prolonged systemic inflammation persistently modifies synaptic plasticity in the hippocampus: modulation by the stress hormones.Microglia and neurodegeneration: the role of systemic inflammation.Review: systemic inflammation and Alzheimer's disease.Protective role of cellular prion protein against TNFα-mediated inflammation through TACE α-secretase.The Role of Microglia in Prion Diseases: A Paradigm of Functional Diversity.Repeated LPS Injection Induces Distinct Changes in the Kynurenine Pathway in Mice.Sodium thiosulphate attenuates brain inflammation induced by systemic lipopolysaccharide administration in C57BL/6J mice.Synergistic effects of NOD1 or NOD2 and TLR4 activation on mouse sickness behavior in relation to immune and brain activity markers.Asiaticoside ameliorates β-amyloid-induced learning and memory deficits in rats by inhibiting mitochondrial apoptosis and reducing inflammatory factors SIRT2 Plays Significant Roles in Lipopolysaccharides-Induced Neuroinflammation and Brain Injury in Mice.Brain Region-dependent Heterogeneity and Dose-dependent Difference in Transient Microglia Population Increase during Lipopolysaccharide-induced Inflammation.Is Delirium the Cognitive Harbinger of Frailty in Older Adults? A Review about the Existing Evidence.

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P2860

Exacerbation of CNS inflammation and neurodegeneration by systemic LPS treatment is independent of circulating IL-1β and IL-6.

http://www.wikidata.org/entity/Q35057271

description

2011 nî lūn-bûn

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2011 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2011 թվականի մայիսին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年论文

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Exacerbation of CNS inflammati ...... of circulating IL-1β and IL-6.

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Exacerbation of CNS inflammati ...... of circulating IL-1β and IL-6.

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Exacerbation of CNS inflammati ...... of circulating IL-1β and IL-6.

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Exacerbation of CNS inflammati ...... of circulating IL-1β and IL-6.

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Exacerbation of CNS inflammati ...... of circulating IL-1β and IL-6.

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Exacerbation of CNS inflammati ...... of circulating IL-1β and IL-6.

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Journal of Neuroinflammation

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Exacerbation of CNS inflammati ...... of circulating IL-1β and IL-6.

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P2093

Carol L Murray

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Colm Cunningham

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Donal T Skelly

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P2860

Systemic inflammatory response reactivates immune-mediated lesions in rat brain.

Systemic inflammation and disease progression in Alzheimer disease.

Lipid A-induced tolerance and hyperreactivity to hypothermia in mice

Cognitive function over time in the Alzheimer's Disease Anti-inflammatory Prevention Trial (ADAPT): results of a randomized, controlled trial of naproxen and celecoxib.

The effect of non-steroidal anti-inflammatory agents on behavioural changes and cytokine production following systemic inflammation: Implications for a role of COX-1

Ligand-induced differentiation of glucocorticoid receptor (GR) trans-repression and transactivation: preferential targetting of NF-kappaB and lack of I-kappaB involvement.

Systemic inflammation induces acute working memory deficits in the primed brain: relevance for delirium.

Hypothermia in systemic inflammation: role of cytokines.

Systemic challenge with the TLR3 agonist poly I:C induces amplified IFNalpha/beta and IL-1beta responses in the diseased brain and exacerbates chronic neurodegeneration

Interleukin (IL)-6 gene expression in the central nervous system is necessary for fever response to lipopolysaccharide or IL-1 beta: a study on IL-6-deficient mice.

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10.1186/1742-2094-8-50

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