LPS receptor (CD14): a receptor for phagocytosis of Alzheimer's amyloid peptide.
about
MyD88 deficiency ameliorates β-amyloidosis in an animal model of Alzheimer's diseaseAmyloidosis in Retinal Neurodegenerative DiseasesMechanisms of Aβ Clearance and Degradation by Glial CellsGenetics ignite focus on microglial inflammation in Alzheimer's diseaseImmune phenotypes of microglia in human neurodegenerative disease: challenges to detecting microglial polarization in human brainsBioenergetic dysfunction and inflammation in Alzheimer's disease: a possible connectionThe proteomics of drusenInnate immunity in Alzheimer's disease: a complex affairGap junctions and hemichannels composed of connexins: potential therapeutic targets for neurodegenerative diseasesNeuroinflammation in Alzheimer's diseaseA Bacterial Component to Alzheimer’s-Type Dementia Seen via a Systems Biology Approach that Links Iron Dysregulation and Inflammagen Shedding to DiseaseThe NALP3 inflammasome is involved in the innate immune response to amyloid-betaMicroglia demonstrate age-dependent interaction with amyloid-β fibrilsMicroglia 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 processesComplement component C3 and complement receptor type 3 contribute to the phagocytosis and clearance of fibrillar Aβ by microgliaLipopolysaccharide-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 diseaseInterleukin-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 pathwayAnnexin 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 diseaseAblation 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 vitroThe 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 cascadeOn 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 studyHippocampal expression of murine IL-4 results in exacerbation of amyloid depositionThe mucosal immune system: master regulator of bidirectional gut-brain communications.Anti-inflammatory activity of low molecular weight polysialic acid on human macrophages.
P2860
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P2860
LPS receptor (CD14): a receptor for phagocytosis of Alzheimer's amyloid peptide.
description
2005 nî lūn-bûn
@nan
2005年の論文
@ja
2005年学术文章
@wuu
2005年学术文章
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2005年学术文章
@zh-cn
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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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
P2093
P2860
P50
P356
P1433
P1476
LPS receptor (CD14): a receptor for phagocytosis of Alzheimer's amyloid peptide
@en
P2093
Botond Penke
Dmitry Cherny
Maryse Letiembre
Silke Walter
Walter Schulz-Schaeffer
P2860
P304
P356
10.1093/BRAIN/AWH531
P407
P577
2005-04-27T00:00:00Z