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mice, tlr, tlrm, pubmed, microglia, tlrw, article, months, brain, ccl, figure, mouse, google, scholar, activation, age, levels, model, cas, deposits, activated, cdb, microglial, amyloid, cerebral, expression, fibrillar, antibody, alzheimers, mrna, disease, mutation, signaling, hippocampus, cells, cytokines, central, monthold, min, water, sections, neocortex, cognitive, chemokines, load, receptor, shown, plaques, deposition, protein,

Topics {✒️}

avidin-biotin immuno-peroxidase method rat anti-tlr4/md2 antibody bone-marrow derived microglia/macrophages bone-marrow derived microglia/monocytes amyloid-beta-induced chemokine production spared long-term memory tgappswe/ps1de9 mice [b6c3-tg open access article article download pdf cells overexpress mip-1alpha avidin-biotin-peroxidase method amyloid-beta peptides induce {beta}-stimulated microglial activation ken-ichiro fukuchi anti-rat igg app[v717i] transgenic mice bio-rad protein assay amyloid-beta peptide oligomerization app/ps1 transgenic mice fibrillar aβ-induced activation appswe/ps1de9 transgenic mice central nervous system cerebral buffer-soluble aβ40 gfap-double-label fluorescence alexa fluoro 488 diminished microglial activation cerebral buffer-soluble aβ42 hong-duck kim cd11b-double-label fluorescence tlr4 wild type wild-type tlr4 buffer-soluble aβ amounts fluorescence-activated cell sorting double-label fluorescence immunohistochemistry aβ42-specific sandwich elisa morris water maze cc chemokine subfamily neurodegenerative diseases hippocampal organotypic cultures homozygous tlr4 mutant related subjects full access rabbit anti-gfap neuroscience research center aβ deposits diminished privacy choices/manage cookies tgappswe/ps1de9 mice specific protein binding authors’ original file 6 pg/mg protein

Questions {❓}

• Wyss-Coray T: Inflammation in Alzheimer disease: driving force, bystander or beneficial response?

Schema {🗺️}

WebPage:
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         headline:TLR4 mutation reduces microglial activation, increases Aβ deposits and exacerbates cognitive deficits in a mouse model of Alzheimer's disease
         description:Amyloid plaques, a pathological hallmark of Alzheimer's disease (AD), are accompanied by activated microglia. The role of activated microglia in the pathogenesis of AD remains controversial: either clearing Aβ deposits by phagocytosis or releasing proinflammatory cytokines and cytotoxic substances. Microglia can be activated via toll-like receptors (TLRs), a class of pattern-recognition receptors in the innate immune system. We previously demonstrated that an AD mouse model homozygous for a loss-of-function mutation of TLR4 had increases in Aβ deposits and buffer-soluble Aβ in the brain as compared with a TLR4 wild-type AD mouse model at 14-16 months of age. However, it is unknown if TLR4 signaling is involved in initiation of Aβ deposition as well as activation and recruitment of microglia at the early stage of AD. Here, we investigated the role of TLR4 signaling and microglial activation in early stages using 5-month-old AD mouse models when Aβ deposits start. Microglial activation and amyloid deposition in the brain were determined by immunohistochemistry in the AD models. Levels of cerebral soluble Aβ were determined by ELISA. mRNA levels of cytokines and chemokines in the brain and Aβ-stimulated monocytes were quantified by real-time PCR. Cognitive functions were assessed by the Morris water maze. While no difference was found in cerebral Aβ load between AD mouse models at 5 months with and without TLR4 mutation, microglial activation in a TLR4 mutant AD model (TLR4M Tg) was less than that in a TLR4 wild-type AD model (TLR4W Tg). At 9 months, TLR4M Tg mice had increased Aβ deposition and soluble Aβ42 in the brain, which were associated with decrements in cognitive functions and expression levels of IL-1β, CCL3, and CCL4 in the hippocampus compared to TLR4W Tg mice. TLR4 mutation diminished Aβ-induced IL-1β, CCL3, and CCL4 expression in monocytes. This is the first demonstration of TLR4-dependent activation of microglia at the early stage of β-amyloidosis. Our results indicate that TLR4 is not involved in the initiation of Aβ deposition and that, as Aβ deposits start, microglia are activated via TLR4 signaling to reduce Aβ deposits and preserve cognitive functions from Aβ-mediated neurotoxicity.
         datePublished:2011-08-09T00:00:00Z
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            Morris Water Maze
            Amyloid Plaque
            TLR4 Signaling
            Escape Platform
            Neurosciences
            Neurology
            Neurobiology
            Immunology
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      headline:TLR4 mutation reduces microglial activation, increases Aβ deposits and exacerbates cognitive deficits in a mouse model of Alzheimer's disease
      description:Amyloid plaques, a pathological hallmark of Alzheimer's disease (AD), are accompanied by activated microglia. The role of activated microglia in the pathogenesis of AD remains controversial: either clearing Aβ deposits by phagocytosis or releasing proinflammatory cytokines and cytotoxic substances. Microglia can be activated via toll-like receptors (TLRs), a class of pattern-recognition receptors in the innate immune system. We previously demonstrated that an AD mouse model homozygous for a loss-of-function mutation of TLR4 had increases in Aβ deposits and buffer-soluble Aβ in the brain as compared with a TLR4 wild-type AD mouse model at 14-16 months of age. However, it is unknown if TLR4 signaling is involved in initiation of Aβ deposition as well as activation and recruitment of microglia at the early stage of AD. Here, we investigated the role of TLR4 signaling and microglial activation in early stages using 5-month-old AD mouse models when Aβ deposits start. Microglial activation and amyloid deposition in the brain were determined by immunohistochemistry in the AD models. Levels of cerebral soluble Aβ were determined by ELISA. mRNA levels of cytokines and chemokines in the brain and Aβ-stimulated monocytes were quantified by real-time PCR. Cognitive functions were assessed by the Morris water maze. While no difference was found in cerebral Aβ load between AD mouse models at 5 months with and without TLR4 mutation, microglial activation in a TLR4 mutant AD model (TLR4M Tg) was less than that in a TLR4 wild-type AD model (TLR4W Tg). At 9 months, TLR4M Tg mice had increased Aβ deposition and soluble Aβ42 in the brain, which were associated with decrements in cognitive functions and expression levels of IL-1β, CCL3, and CCL4 in the hippocampus compared to TLR4W Tg mice. TLR4 mutation diminished Aβ-induced IL-1β, CCL3, and CCL4 expression in monocytes. This is the first demonstration of TLR4-dependent activation of microglia at the early stage of β-amyloidosis. Our results indicate that TLR4 is not involved in the initiation of Aβ deposition and that, as Aβ deposits start, microglia are activated via TLR4 signaling to reduce Aβ deposits and preserve cognitive functions from Aβ-mediated neurotoxicity.
      datePublished:2011-08-09T00:00:00Z
      dateModified:2011-08-09T00:00:00Z
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      sameAs:https://doi.org/10.1186/1742-2094-8-92
      keywords:
         Microglial Activation
         Morris Water Maze
         Amyloid Plaque
         TLR4 Signaling
         Escape Platform
         Neurosciences
         Neurology
         Neurobiology
         Immunology
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      name:Jamaal A Rehman
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            name:Université de Rouen
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            address:
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      name:Department of Medical Genetics, Third Military Medical University, Chongqing, PR China
      name:Department of Cancer Biology and Pharmacology, University of Illinois College of Medicine at Peoria, Peoria, USA
      name:Department of Cancer Biology and Pharmacology, University of Illinois College of Medicine at Peoria, Peoria, USA
      name:Department of Cancer Biology and Pharmacology, University of Illinois College of Medicine at Peoria, Peoria, USA
      name:Department of Cancer Biology and Pharmacology, University of Illinois College of Medicine at Peoria, Peoria, USA
      name:Department of Cancer Biology and Pharmacology, University of Illinois College of Medicine at Peoria, Peoria, USA
      name:Department of Environmental Health Science, New York Medical College, Valhalla, USA
      name:Department of Cancer Biology and Pharmacology, University of Illinois College of Medicine at Peoria, Peoria, USA
      name:CHUM/St-Luc, Neuroscience Research Center, Department of Medicine, University of Montreal, Montreal, Canada
      name:Faculté de Médecine et de Pharmacie, Université de Rouen, Mont Saint Aignan, France
      name:Department of Cancer Biology and Pharmacology, University of Illinois College of Medicine at Peoria, Peoria, USA

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