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000194980 037__ $$aDZNE-2023-00167
000194980 041__ $$aEnglish
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000194980 1001_ $$aShi, Dai$$b0
000194980 245__ $$aThe Anaesthetics Isoflurane and Xenon Reverse the Synaptotoxic Effects of Aβ1-42 on Megf10-Dependent Astrocytic Synapse Elimination and Spine Density in Ex Vivo Hippocampal Brain Slices.
000194980 260__ $$aBasel$$bMolecular Diversity Preservation International$$c2023
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000194980 520__ $$aIt has been hypothesised that inhalational anaesthetics such as isoflurane (Iso) may trigger the pathogenesis of Alzheimer's disease (AD), while the gaseous anaesthetic xenon (Xe) exhibits many features of a putative neuroprotective agent. Loss of synapses is regarded as one key cause of dementia in AD. Multiple EGF-like domains 10 (MEGF10) is one of the phagocytic receptors which assists the elimination of synapses by astrocytes. Here, we investigated how β-amyloid peptide 1-42 (Aβ1-42), Iso and Xe interact with MEGF10-dependent synapse elimination. Murine cultured astrocytes as well as cortical and hippocampal ex vivo brain slices were treated with either Aβ1-42, Iso or Xe and the combination of Aβ1-42 with either Iso or Xe. We quantified MEGF10 expression in astrocytes and dendritic spine density (DSD) in slices. In brain slices of wild type and AAV-induced MEGF10 knock-down mice, antibodies against astrocytes (GFAP), pre- (synaptophysin) and postsynaptic (PSD95) components were used for co-localization analyses by means of immunofluorescence-imaging and 3D rendering techniques. Aβ1-42 elevated pre- and postsynaptic components inside astrocytes and decreased DSD. The combined application with either Iso or Xe reversed these effects. In the presence of Aβ1-42 both anaesthetics decreased MEGF10 expression. AAV-induced knock-down of MEGF10 reduced the pre- and postsynaptic marker inside astrocytes. The presented data suggest Iso and Xe are able to reverse the Aβ1-42-induced enhancement of synaptic elimination in ex vivo hippocampal brain slices, presumably through MEGF10 downregulation.
000194980 536__ $$0G:(DE-HGF)POF4-352$$a352 - Disease Mechanisms (POF4-352)$$cPOF4-352$$fPOF IV$$x0
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000194980 650_7 $$2Other$$aAlzheimer’s disease
000194980 650_7 $$2Other$$aAlzheimer’s disease
000194980 650_7 $$2Other$$aMEGF10
000194980 650_7 $$2Other$$aastrocytes
000194980 650_7 $$2Other$$adendritic spine density
000194980 650_7 $$2Other$$aphagocytosis
000194980 650_7 $$2Other$$asynapse elimination
000194980 650_7 $$2NLM Chemicals$$aamyloid beta-protein (1-42)
000194980 650_7 $$0CYS9AKD70P$$2NLM Chemicals$$aIsoflurane
000194980 650_7 $$03H3U766W84$$2NLM Chemicals$$aXenon
000194980 650_7 $$2NLM Chemicals$$aAmyloid beta-Peptides
000194980 650_7 $$2NLM Chemicals$$aPeptide Fragments
000194980 650_7 $$2NLM Chemicals$$aAnesthetics, Inhalation
000194980 650_7 $$2NLM Chemicals$$aMegf10 protein, mouse
000194980 650_7 $$2NLM Chemicals$$aMembrane Proteins
000194980 650_2 $$2MeSH$$aMice
000194980 650_2 $$2MeSH$$aAnimals
000194980 650_2 $$2MeSH$$aIsoflurane: pharmacology
000194980 650_2 $$2MeSH$$aXenon: pharmacology
000194980 650_2 $$2MeSH$$aXenon: metabolism
000194980 650_2 $$2MeSH$$aAstrocytes: metabolism
000194980 650_2 $$2MeSH$$aAmyloid beta-Peptides: metabolism
000194980 650_2 $$2MeSH$$aBrain: metabolism
000194980 650_2 $$2MeSH$$aHippocampus: metabolism
000194980 650_2 $$2MeSH$$aPeptide Fragments: metabolism
000194980 650_2 $$2MeSH$$aAlzheimer Disease: metabolism
000194980 650_2 $$2MeSH$$aAnesthetics, Inhalation: pharmacology
000194980 650_2 $$2MeSH$$aSynapses: metabolism
000194980 650_2 $$2MeSH$$aMembrane Proteins: metabolism
000194980 7001_ $$aWong, Jaime K Y$$b1
000194980 7001_ $$0P:(DE-2719)2811999$$aZhu, Kaichuan$$b2$$udzne
000194980 7001_ $$00000-0001-9821-8478$$aNoakes, Peter G$$b3
000194980 7001_ $$aRammes, Gerhard$$b4
000194980 770__ $$aAdvance on the Research of Alzheimer's Disease
000194980 773__ $$0PERI:(DE-600)2019364-6$$a10.3390/ijms24020912$$gVol. 24, no. 2, p. 912 -$$n2$$p912$$tInternational journal of molecular sciences$$v24$$x1422-0067$$y2023
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