Chicoric Acid Ameliorated Beta-Amyloid Pathology and Enhanced Expression of Synaptic-Function-Related Markers via L1CAM in Alzheimer's Disease Models.

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  • Additional Information
    • Source:
      Publisher: MDPI Country of Publication: Switzerland NLM ID: 101092791 Publication Model: Electronic Cited Medium: Internet ISSN: 1422-0067 (Electronic) Linking ISSN: 14220067 NLM ISO Abbreviation: Int J Mol Sci Subsets: MEDLINE
    • Publication Information:
      Original Publication: Basel, Switzerland : MDPI, [2000-
    • Subject Terms:
      Alzheimer Disease*/drug therapy ; Alzheimer Disease*/genetics ; Alzheimer Disease*/metabolism ; Neural Cell Adhesion Molecule L1* ; Neurodegenerative Diseases* ; Neuroblastoma* ; Caffeic Acids* ; Succinates*; Humans ; Mice ; Animals ; Amyloid Precursor Protein Secretases/genetics ; Amyloid Precursor Protein Secretases/metabolism ; Amyloid beta-Protein Precursor/metabolism ; Mice, Transgenic ; Disease Models, Animal ; Aspartic Acid Endopeptidases/metabolism ; Amyloid beta-Peptides/metabolism
    • Abstract:
      Alzheimer's disease (AD) is the most common progressive neurodegenerative disease. The accumulation of amyloid-beta (Aβ) plaques is a distinctive pathological feature of AD patients. The aims of this study were to evaluate the therapeutic effect of chicoric acid (CA) on AD models and to explore its underlying mechanisms. APPswe/Ind SH-SY5Y cells and 5xFAD mice were treated with CA. Soluble Aβ1-42 and Aβ plaque levels were analyzed by ELISA and immunohistochemistry, respectively. Transcriptome sequencing was used to compare the changes in hippocampal gene expression profiles among the 5xFAD mouse groups. The specific gene expression levels were quantified by qRT-PCR and Western blot analysis. It was found that CA treatment reduced the Aβ1-42 levels in the APPswe/Ind cells and 5xFAD mice. It also reduced the Aβ plaque levels as well as the APP and BACE1 levels. Transcriptome analysis showed that CA affected the synaptic-plasticity-related genes in the 5xFAD mice. The levels of L1CAM, PSD-95 and synaptophysin were increased in the APPswe/Ind SH-SY5Y cells and 5xFAD mice treated with CA, which could be inhibited by administering siRNA-L1CAM to the CA-treated APPswe/Ind SH-SY5Y cells. In summary, CA reduced Aβ levels and increased the expression levels of synaptic-function-related markers via L1CAM in AD models.
      Competing Interests: The authors declare no conflicts of interest.
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    • Grant Information:
      2022JJ12SN050 Dalian Science and Technology Innovation Fund Project; 2022RG09 Innovation and Entrepreneurship Plan of Science and technology Talent of Dalian; Youth Talent Cultivation Fund Project of Dalian Medical University Youth Talent Cultivation Fund Project of Dalian Medical University
    • Contributed Indexing:
      Keywords: Alzheimer’s disease; L1CAM; amyloid-β plaques; chicoric acid; synaptic plasticity
    • Accession Number:
      EC 3.4.- (Amyloid Precursor Protein Secretases)
      S4YY3V8YHD (chicoric acid)
      0 (Neural Cell Adhesion Molecule L1)
      0 (Amyloid beta-Protein Precursor)
      EC 3.4.23.- (Aspartic Acid Endopeptidases)
      0 (Amyloid beta-Peptides)
      0 (Caffeic Acids)
      0 (Succinates)
    • Publication Date:
      Date Created: 20240328 Date Completed: 20240329 Latest Revision: 20240330
    • Publication Date:
      20240330
    • Accession Number:
      PMC10970381
    • Accession Number:
      10.3390/ijms25063408
    • Accession Number:
      38542381