國家衛生研究院 NHRI:Item 3990099045/15259
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 12145/12927 (94%)
Visitors : 851653      Online Users : 968
RC Version 6.0 © 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
    Home ‧ Login ‧ Upload ‧ Help ‧ About ‧ Administer Goto mobile version


    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/15259


    Title: Gliptins normalize posttraumatic hippocampal neurogenesis and restore cognitive function after controlled cortical impact on sensorimotor cortex
    Authors: Hung, YW;Lu, GL;Chen, HH;Tung, HH;Lee, SL
    Contributors: Institute of Cellular and Systems Medicine;Center for Neuropsychiatric Research
    Abstract: Traumatic brain injury (TBI) often leads to long-term neurocognitive dysfunctions. Adult neurogenesis in the hippocampal dentate gyrus (DG) serves critical functions in cognition but can be disrupted by brain injury and insult in serval forms. In the present study, we explore the cellular and molecular targets of DPP-4 inhibitors (or gliptins) as related to hippocampal function and TBI cognitive sequelae. Two structurally different gliptins, sitagliptin and vildagliptin, were examined using a controlled cortical impact (CCI) model of moderate TBI in mice. Sensorimotor CCI, although distal from the hippocampus, impaired hippocampal-dependent cognition without obvious hippocampal tissue destruction. Neurogenic cell proliferation in the DG was increased accompanied by large numbers of reactive astrocyte. Increased numbers of immature granule cells with abnormal dendritic outgrowth were ectopically localized in the outer granule cell layer (GCL) and hilus. Long-term potentiation of dentate immature granule cells was also impaired. Both sitagliptin and vildagliptin attenuated the CCI-induced ectopic migration of doublecortin-positive immature neurons into the outer GCL and hilus, restored the normal dendritic branching pattern of the immature neurons and prevented astrocyte reactivation. Both gliptins prevented loss of normal synaptic integration in the DG after sensorimotor CCI and improved cognitive behavior. Sensorimotor cortical injury thus results in an abnormal neurogenesis pattern and astrocyte reactivation in the distal hippocampus which appears to contribute to the development of cognitive dysfunction after TBI. DPP-4 inhibitors prevent astrocyte reactivation, normalize the posttraumatic hippocampal neurogenesis and help to maintain normal electrophysiology in the DG with positive behavioral effect in a mouse model.
    Date: 2023-09
    Relation: Biomedicine and Pharmacotherapy. 2023 Sep;165:Article number 115270.
    Link to: http://dx.doi.org/10.1016/j.biopha.2023.115270
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0753-3322&DestApp=IC2JCR
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85167426537
    Appears in Collections:[Sheau-Ling Lee] Periodical Articles
    [Hwei-Hisen Chen] Periodical Articles

    Files in This Item:

    File Description SizeFormat
    SCP85167426537.pdf15749KbAdobe PDF141View/Open


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

    Related Items in TAIR

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