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Upregulation of TREM2 Ameliorates Neuroinflammatory Responses and Improves Cognitive Deficits Triggered by Surgical

Yanhua Jiang1, Zhe Li1, Hong Ma1

  • 1Department of Anesthesiology, the First Hospital of China Medical University, Shenyang, China.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|April 25, 2018
PubMed
Abstract

Insights

Downregulation of TREM2 worsened surgery-induced cognitive decline and neuroinflammation in Alzheimer

Area of Science:

  • Neuroscience
  • Immunology
  • Genetics

Background:

  • The TREM2 (triggering receptor expressed on myeloid cells 2) pathway, involving DAP12, is critical for microglial function.
  • TREM2 can suppress neuroinflammation by reducing microglia-driven cytokine production.
  • Surgery-induced cognitive deficits and neuroinflammation are significant concerns, particularly in Alzheimer's disease models.

Purpose of the Study:

  • To investigate the role of TREM2 in surgery-induced cognitive deficits and neuroinflammation.
  • To examine the effects of TREM2 modulation in wild-type (WT) and APPswe/PS1dE9 mice, a model for Alzheimer's disease.

Main Methods:

  • Adult male APPswe/PS1dE9 transgenic and WT mice received intracerebral lentiviral particles encoding mouse TREM2.
  • Mice underwent partial hepatectomy 1 month post-injection.
  • Behavioral tests (open-field, Morris water maze), and hippocampal analyses (TREM2, DAP12, IL-1β, Iba-1, Arg1, synaptophysin, tau phosphorylation, GSK-3β) were performed.

Main Results:

  • Surgery exacerbated cognitive impairment and IL-1β in transgenic mice, correlating with decreased TREM2 levels.
  • TREM2 overexpression downregulated IL-1β, reduced tau hyperphosphorylation (T396), inhibited GSK-3β activity, and improved behavior.
  • TREM2 overexpression increased Arg1 and synaptophysin levels in the hippocampus of transgenic mice.

Conclusions:

  • Downregulation of TREM2 exacerbates surgery-induced cognitive deficits and neuroinflammation in this Alzheimer's disease model.
  • TREM2 overexpression attenuates these negative effects by reducing pro-inflammatory cytokines, inhibiting tau pathology, and enhancing synaptic markers.
Keywords:
CytokinesHippocampusMicrogliaNeuroinflammationPostoperative Cognitive Dysfunction (POCD)Trem2

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