LPS receptor (CD14): a receptor for phagocytosis of Alzheimer's amyloid peptide. - Wikidata - wikimedia - TriplyDB

LPS receptor (CD14): a receptor for phagocytosis of Alzheimer's amyloid peptide.

LPS receptor (CD14): a receptor for phagocytosis of Alzheimer's amyloid peptide.

http://www.wikidata.org/entity/Q51817662

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MyD88 deficiency ameliorates β-amyloidosis in an animal model of Alzheimer's disease Amyloidosis in Retinal Neurodegenerative Diseases Mechanisms of Aβ Clearance and Degradation by Glial Cells Genetics ignite focus on microglial inflammation in Alzheimer's disease Immune phenotypes of microglia in human neurodegenerative disease: challenges to detecting microglial polarization in human brains Bioenergetic dysfunction and inflammation in Alzheimer's disease: a possible connection The proteomics of drusen Innate immunity in Alzheimer's disease: a complex affair Gap junctions and hemichannels composed of connexins: potential therapeutic targets for neurodegenerative diseases Neuroinflammation in Alzheimer's disease A Bacterial Component to Alzheimer’s-Type Dementia Seen via a Systems Biology Approach that Links Iron Dysregulation and Inflammagen Shedding to Disease The NALP3 inflammasome is involved in the innate immune response to amyloid-beta Microglia demonstrate age-dependent interaction with amyloid-β fibrils Microglia activated with the toll-like receptor 9 ligand CpG attenuate oligomeric amyloid {beta} neurotoxicity in in vitro and in vivo models of Alzheimer's disease.Inefficient clearance of myelin debris by microglia impairs remyelinating processes Complement component C3 and complement receptor type 3 contribute to the phagocytosis and clearance of fibrillar Aβ by microglia Lipopolysaccharide-induced cerebral inflammatory damage and the therapeutic effect of platelet activating factor receptor antagonist.Involvement of the Bradykinin B1 Receptor in Microglial Activation: In Vitro and In Vivo Studies.Inflammation, microglia, and Alzheimer's disease.Phagocytosis and LPS alter the maturation state of β-amyloid precursor protein and induce different Aβ peptide release signatures in human mononuclear phagocytes.Deletion of CD14 attenuates Alzheimer's disease pathology by influencing the brain's inflammatory milieu.MyD88 is dispensable for cerebral amyloidosis and neuroinflammation in APP/PS1 transgenic mice.Temporal gene profiling of the 5XFAD transgenic mouse model highlights the importance of microglial activation in Alzheimer's disease.Toll-like receptors in Alzheimer's disease Interleukin-1 receptor 1 knockout has no effect on amyloid deposition in Tg2576 mice and does not alter efficacy following Abeta immunotherapy.Activation of BV2 microglia by lipopolysaccharide triggers an inflammatory reaction in PC12 cell apoptosis through a toll-like receptor 4-dependent pathway Annexin A1: a central player in the anti-inflammatory and neuroprotective role of microglia.Toll-like receptor 4 promotes α-synuclein clearance and survival of nigral dopaminergic neurons.TLR4 mutation reduces microglial activation, increases Aβ deposits and exacerbates cognitive deficits in a mouse model of Alzheimer's disease Ablation of TNF-RI/RII expression in Alzheimer's disease mice leads to an unexpected enhancement of pathology: implications for chronic pan-TNF-α suppressive therapeutic strategies in the brain.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.Resveratrol mitigates lipopolysaccharide- and Aβ-mediated microglial inflammation by inhibiting the TLR4/NF-κB/STAT signaling cascade On the translocation of bacteria and their lipopolysaccharides between blood and peripheral locations in chronic, inflammatory diseases: the central roles of LPS and LPS-induced cell death.Genetics of CD33 in Alzheimer's disease and acute myeloid leukemia.The biphasic role of microglia in Alzheimer's disease.Extensive innate immune gene activation accompanies brain aging, increasing vulnerability to cognitive decline and neurodegeneration: a microarray study Hippocampal expression of murine IL-4 results in exacerbation of amyloid deposition The mucosal immune system: master regulator of bidirectional gut-brain communications.Anti-inflammatory activity of low molecular weight polysialic acid on human macrophages.

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LPS receptor (CD14): a receptor for phagocytosis of Alzheimer's amyloid peptide.

http://www.wikidata.org/entity/Q51817662

description

2005 nî lūn-bûn

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2005年の論文

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2005年学术文章

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2005年学术文章

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2005年学术文章

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2005年学术文章

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2005年学术文章

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2005年学术文章

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2005年學術文章

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2005年學術文章

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name

LPS receptor (CD14): a receptor for phagocytosis of Alzheimer's amyloid peptide.

@en

LPS receptor

@nl

type

label

LPS receptor (CD14): a receptor for phagocytosis of Alzheimer's amyloid peptide.

@en

LPS receptor

@nl

prefLabel

LPS receptor (CD14): a receptor for phagocytosis of Alzheimer's amyloid peptide.

@en

LPS receptor

@nl

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P1476

LPS receptor (CD14): a receptor for phagocytosis of Alzheimer's amyloid peptide

@en

P2093

Botond Penke

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

Dmitry Cherny

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

Maryse Letiembre

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

Silke Walter

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

Walter Schulz-Schaeffer

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Yang Liu

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P2860

Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein

Resistance to endotoxin shock and reduced dissemination of gram-negative bacteria in CD14-deficient mice

Human CD14 mediates recognition and phagocytosis of apoptotic cells

Immunization with amyloid-beta attenuates Alzheimer-disease-like pathology in the PDAPP mouse

Fluorescence resonance energy transfer determinations using multiphoton fluorescence lifetime imaging microscopy to characterize amyloid-beta plaques.

A beta peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease.

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

Simvastatin strongly reduces levels of Alzheimer's disease beta -amyloid peptides Abeta 42 and Abeta 40 in vitro and in vivo.

Fluorescence energy transfer as a spectroscopic ruler.

CD14 signalling in lipid rafts: new ligands and co-receptors.

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1778-1789

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scholarly article

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10.1093/BRAIN/AWH531

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Pt 8

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128

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Klaus Fassbender

Massimiliano Stagi

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2005-04-27T00:00:00Z

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7880020

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15857927

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