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Related Experiment Video

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CD33 Ameliorates Surgery-Induced Spatial Learning and Memory Impairments Through TREM2.

Jie Zou1,2, Yaxuan Wang1, Xinyue Zhang1

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

Molecular Neurobiology
|August 1, 2024
PubMed
Summary

Targeting CD33, a protein implicated in neuroinflammation, can prevent cognitive decline after surgery. Inhibiting CD33 in aged mice improved memory and reduced inflammatory responses, suggesting a new therapeutic approach for postoperative cognitive dysfunction (POCD).

Keywords:
AnesthesiaCD33HepatectomyNeuroinflammationPOCDSurgeryTREM2

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Area of Science:

  • Neuroscience
  • Immunology
  • Gerontology

Background:

  • Neuroinflammation is a key factor in postoperative cognitive dysfunction (POCD).
  • CD33 and TREM2 are critical in regulating immune responses and neuroinflammation.
  • Understanding their roles is vital for addressing cognitive deficits after surgery.

Purpose of the Study:

  • To investigate the impact of CD33 and TREM2 on POCD in aged mice.
  • To explore the potential of targeting CD33 as a therapeutic strategy for POCD.

Main Methods:

  • Aged mice underwent partial hepatectomy and cognitive assessments using the Morris water maze.
  • siRNA was used to modulate CD33 and TREM2 expression in vivo and in BV2 microglia cells.
  • Quantitative RT-PCR and western blot analyzed gene and protein expression.

Main Results:

  • Surgery and anesthesia increased CD33 expression, causing spatial learning and memory impairments.
  • CD33 inhibition via siRNA ameliorated cognitive deficits and reduced neuroinflammation.
  • CD33 knockdown suppressed pro-inflammatory cytokines, suggesting CD33 promotes neuroinflammation by inhibiting TREM2.

Conclusions:

  • CD33 plays a significant role in the development of POCD by exacerbating neuroinflammation.
  • Targeting CD33 offers a promising therapeutic avenue for preventing and treating POCD.
  • CD33 may influence cognitive function and neuroinflammation through TREM2-dependent pathways.