Skip to content
DraconiticResearch
Search Sources API
201,818 studies31 sourcesUpdated 30 min ago
Peer-reviewedCC BYNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics

Overexpression of hippocampal AdipoR1 ameliorates cognitive dysfunction in APP/PS1 mice through inhibiting NLRP3-Mediated neuronal pyroptosis

  • Chunnian Hu1
  • Jing Li1
  • Lin Jiang2
  • Yuning Zhou1
  • Yuhui Deng1
  • Qing Pan1
  • Shun Wang1
  • Wenyu Yang1
  • Lei Zhang1
  • Fenglei Chao1
  • Yanmin Luo3
  • Jing Tang1
5 more authors
  • Qian Xiao3
  • Xin Liang3
  • Yingqiang Qi1
  • Yong Tang1
  • Chunni Zhou1
  1. 1Department of Histology and Embryology, College of Basic Medicine, Chongqing Medical University, Chongqing, China
  2. 2Lab Teaching & Management Center, Chongqing Medical University, Chongqing, China
  3. 3Laboratory of Stem Cells and Tissue Engineering, College of Basic Medicine, Chongqing Medical University, Chongqing, China
Read full textPDFDOICite

Abstract

Alzheimer’s disease (AD) is a prevalent neurodegenerative disorder primarily characterized by progressive cognitive dysfunction. Substantial loss of hippocampal neurons is closely associated with irreversible cognitive decline; however, the underlying mechanisms have not yet been fully elucidated. In this study, conditionally overexpressing adiponectin receptor 1 (AdipoR1) in the hippocampus of APP/PS1 transgenic AD mice, we found that it significantly improved learning and memory abilities and effectively mitigated the abnormal loss of hippocampal neurons and dendritic spines. AdipoR1 overexpression primarily maintained neuronal numbers through reducing neuronal death rather than promoting neurogenesis, and this protective effect is closely linked to the inhibition of the neuronal NLRP3 inflammasome, leading to a marked reduction in pyroptosis levels within the hippocampus. Our results demonstrated, for the first time, that AdipoR1 exerted a crucial neuroprotective role in AD pathology through modulating the NLRP3-mediated neuroinflammatory pathway, which might offer new insights into the mechanisms of neuronal loss in AD and suggest that the AdipoR1–NLRP3 signaling axis may serve as a potential therapeutic target for early intervention in AD.

Related

  1. Treadmill Exercise Attenuates Hippocampal Neuroinflammation and Ameliorates Cognitive Dysfunction in Methamphetamine-Addicted Mice: Transcriptomic Screening Identifies NLRC5 as a Candidate Molecule
    YING Guo-Si, HUANG Qiu-Yue, XU Ji-Sheng +3
    Shengwu huaxue yu shengwu wuli jinzhanPeer-reviewedCC BY-NCFull textNeurologyDOAJ
  2. Xinfeng capsule regulates pyroptosis and ameliorates cardiac fibrosis in rheumatoid arthritis through lncRNA GAS5 and TLR4/ROS/miR-21 pathways
    Hui Wang, Wanlan Fu, Yunxiang Cao +3
    Annals of medicine and surgery (2012)Peer-reviewedCC BY-NC-NDFull textGeneral medicineEurope PMC
  3. Mild heat treatment ameliorates PCOS by activating PI3K/Akt signaling and inhibiting granulosa cell apoptosis
    Zhe Yang, Qixuan Zhang, Xiangyang Ou +6
    Scientific ReportsPeer-reviewedCC BY-NC-ND 4.0Full textObstetrics, gynaecology & paediatricsCrossref
  4. BMI1 Overexpression Alleviates Metabolic Syndrome‐Related Liver Injury by Inhibiting the Activation of the METTL3/AHNAK Axis
    Yun‐Jiang Chen, Bei Song, Kai‐Yu Cai +2
    The Kaohsiung Journal of Medical SciencesPeer-reviewedCC BY 4.0Full textEpidemiology & public healthPMCEurope PMC
  5. Hepatic Overexpression of Lysophospholipid Acyltransferase LPLAT14/MBOAT1 Ameliorates Mild Liver Injury During Early High‐Fat Diet Feeding
    Sho Hori, Kahori Shimizu, Taiga Kikuchi +5
    FASEB bioAdvancesPeer-reviewedCC BYFull textEpidemiology & public healthEurope PMCPMCEurope PMC

Cite

BibTeXRIS
BibTeX
@article{hu2026overexpression,
  title = {{Overexpression of hippocampal AdipoR1 ameliorates cognitive dysfunction in APP/PS1 mice through inhibiting NLRP3-Mediated neuronal pyroptosis}},
  author = {Chunnian Hu and Jing Li and Lin Jiang and Yuning Zhou and Yuhui Deng and Qing Pan and Shun Wang and Wenyu Yang and Lei Zhang and Fenglei Chao and Yanmin Luo and Jing Tang and Qian Xiao and Xin Liang and Yingqiang Qi and Yong Tang and Chunni Zhou},
  journal = {Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics},
  year = {2026},
  month = oct,
  doi = {10.1016/j.neurot.2026.e01093},
  url = {https://europepmc.org/article/PMC/PMC13722108},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Overexpression of hippocampal AdipoR1 ameliorates cognitive dysfunction in APP/PS1 mice through inhibiting NLRP3-Mediated neuronal pyroptosis
AU  - Chunnian Hu
AU  - Jing Li
AU  - Lin Jiang
AU  - Yuning Zhou
AU  - Yuhui Deng
AU  - Qing Pan
AU  - Shun Wang
AU  - Wenyu Yang
AU  - Lei Zhang
AU  - Fenglei Chao
AU  - Yanmin Luo
AU  - Jing Tang
AU  - Qian Xiao
AU  - Xin Liang
AU  - Yingqiang Qi
AU  - Yong Tang
AU  - Chunni Zhou
PY  - 2026
DA  - 2026/10/26
JO  - Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics
DO  - 10.1016/j.neurot.2026.e01093
UR  - https://europepmc.org/article/PMC/PMC13722108
AB  - Alzheimer’s disease (AD) is a prevalent neurodegenerative disorder primarily characterized by progressive cognitive dysfunction. Substantial loss of hippocampal neurons is closely associated with irreversible cognitive decline; however, the underlying mechanisms have not yet been fully elucidated. In this study, conditionally overexpressing adiponectin receptor 1 (AdipoR1) in the hippocampus of APP/PS1 transgenic AD mice, we found that it significantly improved learning and memory abilities and effectively mitigated the abnormal loss of hippocampal neurons and dendritic spines. AdipoR1 overexpression primarily maintained neuronal numbers through reducing neuronal death rather than promoting neurogenesis, and this protective effect is closely linked to the inhibition of the neuronal NLRP3 inflammasome, leading to a marked reduction in pyroptosis levels within the hippocampus. Our results demonstrated, for the first time, that AdipoR1 exerted a crucial neuroprotective role in AD pathology through modulating the NLRP3-mediated neuroinflammatory pathway, which might offer new insights into the mechanisms of neuronal loss in AD and suggest that the AdipoR1–NLRP3 signaling axis may serve as a potential therapeutic target for early intervention in AD.
SN  - 1933-7213
SN  - 1878-7479
ER  -