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A Mouse Model of Orthopedic Surgery to Study Postoperative Cognitive Dysfunction and Tissue Regeneration
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Neutrophils: a new target for postoperative cognitive dysfunction.

Jianxin Cheng1, Jin Gao2, Jianjun Li3

  • 1Department of Anesthesiology, Cheeloo College of Medicine, Qilu Hospital (Qingdao), Shandong University, Qingdao, 266035, China.

Apoptosis : an International Journal on Programmed Cell Death
|March 5, 2025
PubMed
Summary

Postoperative cognitive dysfunction (POCD) involves brain inflammation triggered by surgical stress. Neutrophils play a key role in POCD pathogenesis by promoting neuroinflammation and altering blood-brain barrier permeability.

Keywords:
InflammationNETsNeutrophilPostoperative cognitive dysfunction

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Area of Science:

  • Neuroscience
  • Immunology
  • Geriatric Medicine

Background:

  • Postoperative cognitive dysfunction (POCD) is a common central nervous system complication after surgery, especially in the elderly.
  • Surgical stress and anesthesia can induce systemic inflammation, leading to neuroinflammation and cognitive decline.
  • Neutrophils are key immune cells implicated in the inflammatory pathways contributing to POCD.

Purpose of the Study:

  • To systematically review recent findings on neutrophil functions in the context of POCD.
  • To explore the role of neutrophils in neuroinflammation and blood-brain barrier alterations following surgery.
  • To offer new perspectives for POCD research and clinical interventions.

Main Methods:

  • Systematic literature review of recent research on neutrophils and POCD.
  • Analysis of studies investigating neutrophil activation, cytokine/chemokine secretion, and NET formation.
  • Examination of research on neutrophil-mediated blood-brain barrier permeability changes.

Main Results:

  • Neutrophils are rapidly activated peripherally, releasing inflammatory mediators and neutrophil extracellular traps (NETs).
  • Neutrophil infiltration into the brain contributes significantly to neuroinflammation in POCD.
  • Neutrophils can increase blood-brain barrier permeability, exacerbating cognitive impairment.

Conclusions:

  • Neutrophils are critical effectors in the pathogenesis of POCD.
  • Understanding neutrophil functions provides a basis for developing targeted therapies for POCD.
  • Further research into neutrophil mechanisms can optimize clinical strategies for preventing and treating POCD.