Absence of detectable IL-1beta production in murine prion disease: a model of chronic neurodegeneration.
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Prion pathogenesis in the absence of NLRP3/ASC inflammasomesAnti-prion activity of Brilliant Blue GNLRP3 inflammasome activation in macrophage cell lines by prion protein fibrils as the source of IL-1β and neuronal toxicity.Microglia and the urokinase plasminogen activator receptor/uPA system in innate brain inflammation.Subtype and regional-specific neuroinflammation in sporadic creutzfeldt-jakob disease.Morphological and functional abnormalities in mitochondria associated with synaptic degeneration in prion disease.Prion pathogenesis in the absence of Toll-like receptor signallingExacerbation of CNS inflammation and neurodegeneration by systemic LPS treatment is independent of circulating IL-1β and IL-6.The acute inflammatory response to intranigral α-synuclein differs significantly from intranigral lipopolysaccharide and is exacerbated by peripheral inflammation.Toll-like receptors in chronic pain.Microglia in the degenerating brain are capable of phagocytosis of beads and of apoptotic cells, but do not efficiently remove PrPSc, even upon LPS stimulation.Defining the Microglia Response during the Time Course of Chronic NeurodegenerationSystemic inflammation induces acute behavioral and cognitive changes and accelerates neurodegenerative disease.Analysis of protein levels of 24 cytokines in scrapie agent-infected brain and glial cell cultures from mice differing in prion protein expression levelsThe more you have, the less you get: the functional role of inflammation on neuronal differentiation of endogenous and transplanted neural stem cells in the adult brain.A review of postoperative cognitive dysfunction and neuroinflammation associated with cardiac surgery and anaesthesia.Microglia and neurodegeneration: the role of systemic inflammation.Prion disease and the innate immune system.Role of interleukin-1 in prion disease-associated astrocyte activation.The Role of Microglia in Prion Diseases: A Paradigm of Functional Diversity.Microglia in prion diseases.Pain intensity and duration can be enhanced by prior challenge: initial evidence suggestive of a role of microglial primingComparison of inflammatory and acute-phase responses in the brain and peripheral organs of the ME7 model of prion diseaseTransforming growth factor-beta 1-mediated neuroprotection against excitotoxic injury in vivo.Prolonged exposure of microglia to lipopolysaccharide modifies the intracellular signaling pathways and selectively promotes prostaglandin E2 synthesis.Neuropil and neuronal changes in hippocampal NADPH-diaphorase histochemistry in the ME7 model of murine prion disease.Monocyte chemoattractant protein-1 deficiency is protective in a murine stroke model.
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P2860
Absence of detectable IL-1beta production in murine prion disease: a model of chronic neurodegeneration.
description
2001 nî lūn-bûn
@nan
2001年の論文
@ja
2001年学术文章
@wuu
2001年学术文章
@zh
2001年学术文章
@zh-cn
2001年学术文章
@zh-hans
2001年学术文章
@zh-my
2001年学术文章
@zh-sg
2001年學術文章
@yue
2001年學術文章
@zh-hant
name
Absence of detectable IL-1beta ...... of chronic neurodegeneration.
@en
Absence of detectable IL-1beta ...... of chronic neurodegeneration.
@nl
type
label
Absence of detectable IL-1beta ...... of chronic neurodegeneration.
@en
Absence of detectable IL-1beta ...... of chronic neurodegeneration.
@nl
prefLabel
Absence of detectable IL-1beta ...... of chronic neurodegeneration.
@en
Absence of detectable IL-1beta ...... of chronic neurodegeneration.
@nl
P2093
P2860
P356
P1476
Absence of detectable IL-1beta ...... of chronic neurodegeneration.
@en
P2093
P2860
P304
P356
10.1093/JNEN/60.2.173
P577
2001-02-01T00:00:00Z