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ORIGINAL RESEARCH article

Front. Immunol.
Sec. Multiple Sclerosis and Neuroimmunology
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1555124
This article is part of the Research Topic Remedying the injured brain in cognitive impairment: potential neuroimmune communication signaling and therapeutic opportunities View all 5 articles

The changes of NLRs family members in the brain of AD mouse model and AD patients

Provisionally accepted
Zehan Li Zehan Li 1Yanling He Yanling He 2Jingdan Zhang Jingdan Zhang 3Jing Yang Jing Yang 4Jinbo Cheng Jinbo Cheng 5*Zhang Xuewu Zhang Xuewu 1*
  • 1 Yanbian University, Yanji, Jilin, China
  • 2 Anhui Medical University, Hefei, Anhui Province, China
  • 3 Beijing Institute of Basic Medical Sciences, Beijing, China
  • 4 Hebei Medical University, Shijiazhuang, Hebei Province, China
  • 5 College of Life and Environmental Sciences, Minzu University of China, Beijing, China

The final, formatted version of the article will be published soon.

    Alzheimer's disease (AD), a prevalent neurodegenerative disease, is primarily characterized by progressive neuron loss and memory impairment. NOD-like receptors (NLRs) are crucial for immune regulation and maintaining cellular homeostasis. Recently, NLRs have been identified as important contributors to neuroinflammation, thus presenting a potential approach for reducing inflammation and slowing AD progression. In this study, we examined the expression of NLR family members in the human AD database, and found increased levels of CIITA, NOD1, NLRC5, NLRP1, NLRP3, NLRP7, NLRP10, NLRP12, and NLRP13 in hippocampus tissue in patients with AD, along with increased levels of NOD1, NLRC5, NLRX1, NLRP3, and NLRP7 levels in frontal cortex tissue. Furthermore, through detecting their levels in AD mouse model, we found that NLRP3 levels were significantly increased. Additionally, we found that NLRP3 expressions were mainly elevated in microglia surrounding Aβ plaques in AD mouse model and human AD patients. These findings highlight the potential important role of NLRP3 in AD pathology, offering new therapeutic targets and interventions.

    Keywords: Alzheimer's disease, NLRs, NLRP3, Microglia, Aβ plaques

    Received: 03 Jan 2025; Accepted: 05 Feb 2025.

    Copyright: © 2025 Li, He, Zhang, Yang, Cheng and Xuewu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Jinbo Cheng, College of Life and Environmental Sciences, Minzu University of China, Beijing, China
    Zhang Xuewu, Yanbian University, Yanji, 133002, Jilin, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.