English  |  正體中文  |  简体中文  |  Items with full text/Total items : 17918/22933 (78%)
Visitors : 7416866      Online Users : 53
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
  • Adv. Search
    HomeLoginUploadHelpAboutAdminister Goto mobile version
    CSMUIR > researcher portal > Artical >  Item 310902500/23976
    Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/23976


    Title: Neuroprotective Effects of Ceftriaxone Involve the Reduction of A beta Burden and Neuroinflammatory Response in a Mouse Model of Alzheimer's Disease
    Authors: Tikhonova, MA;Amstislavskaya, TG;Ho, YJ;Akopyan, AA;Tenditnik, MV;Ovsyukova, MV;Bashirzade, AA;Dubrovina, NI;Aftanas, LI
    Keywords: neurodegeneration;drug repurposing;amyloid;microglia;cognition;behavior
    Date: 2021
    Issue Date: 2022-08-05T09:45:50Z (UTC)
    Publisher: FRONTIERS MEDIA SA
    Abstract: Ceftriaxone (CEF) is a safe and multipotent antimicrobial agent that possesses neuroprotective properties. Earlier, we revealed the restoration of cognitive function in OXYS rats with signs of Alzheimer's disease (AD)-like pathology by CEF along with its modulating the expression of genes related to the system of amyloid beta (A beta) metabolism in the brain. The aim of this study was to determine the effects of CEF on behavior, A beta deposition, and associated neuroinflammation using another model of an early AD-like pathology induced by A beta. Mice were injected bilaterally i.c.v. with A beta fragment 25-35 to produce the AD model, while the CEF treatment (100 mg/kg/day, i.p., 36 days) started the next day after the surgery. The open field test, T-maze, Barnes test, IntelliCage, and passive avoidance test were used for behavioral phenotyping. Neuronal density, amyloid accumulation, and the expression of neuroinflammatory markers were measured in the frontal cortex and hippocampus. CEF exhibited beneficial effects on some cognitive features impaired by A beta neurotoxicity including complete restoration of the fear-induced memory and learning in the passive avoidance test and improved place learning in the IntelliCage. CEF significantly attenuated amyloid deposition and neuroinflammatory response. Thus, CEF could be positioned as a potent multipurpose drug as it simultaneously targets proteostasis network and neuroinflammation, as well as glutamate excitotoxicity, oxidative pathways, and neurotrophic function as reported earlier. Together with previous reports on the positive effects of CEF in AD models, the results confirm the potential of CEF as a promising treatment against cognitive decline from the early stages of AD progression.</p>
    URI: http://dx.doi.org/10.3389/fnins.2021.736786
    https://www.webofscience.com/wos/woscc/full-record/WOS:000717225700001
    https://ir.csmu.edu.tw:8080/handle/310902500/23976
    Relation: FRONTIERS IN NEUROSCIENCE ,2021,v15
    Appears in Collections:[researcher portal] Artical

    Files in This Item:

    File Description SizeFormat
    index.html0KbHTML199View/Open


    SFX Query

    All items in CSMUIR are protected by copyright, with all rights reserved.


    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback