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Original Research ARTICLE Provisionally accepted The full-text will be published soon. Notify me

Front. Aging Neurosci. | doi: 10.3389/fnagi.2019.00279

Immune system drives synapse loss during LPS-induced learning and memory impairment in mice

 Yirong Xin1, 2,  Junxing Jiang2,  YANG HU2, Junping Pan2, Xiangnan Mi2, Qin Gao2,  Fei Xiao2*, Wei Zhang3* and  Huanmin Luo2*
  • 1Jinan University, China
  • 2Department of pharmacology, College of Basic Medicine, Jinan University, China
  • 3Ningxia Medical University, China

Although lipopolysaccharides (LPS) have been used to induce an Alzheimer’s disease like animal model, the exact mechanisms involved have not been studied. This study was designed to confirm an animal model of learning and memory impairment induced by LPS, and explore which biological processes and pathways have taken part in it. Mice were continuously intraperitoneally injected with LPS for 7 days. Learning and memory related behavioral and pathological performances were tested by Morris water maze and immunostaining respectively. The expressions of C1q, C3, microglia and their regulators-cytokines were comprehensively detected. After 7 days of administration, LPS induced learning and memory disorder in mice, which is attributed to neural impairment and synapse loss in hippocampus. The immune system was activated, in which classical complement pathway and microglia phagocytosis were shown to be involved in the synapse loss. LPS-injected mouse can serve as an early memory impairment model for anti-AD drugs researches.

Keywords: lipopolysac charides, Learning and memory impairment, Neuroinflammation, complement, Microglia

Received: 13 May 2019; Accepted: 30 Sep 2019.

Copyright: © 2019 Xin, Jiang, HU, Pan, Mi, Gao, Xiao, Zhang and Luo. 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) and the copyright owner(s) 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:
Dr. Fei Xiao, Department of pharmacology, College of Basic Medicine, Jinan University, Guangzhou, China,
Mx. Wei Zhang, Ningxia Medical University, Yinchuan, China,
Prof. Huanmin Luo, Department of pharmacology, College of Basic Medicine, Jinan University, Guangzhou, China,