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A decrease in NR2B expression mediated by DNA hypermethylation induces perioperative neurocognitive disorder in aged

Feifei Xu1, Peilin Cong2, Bingqian Zhang3

  • 1Department of Anesthesiology and Perioperative Medicine, Xijing Hospital, Fourth Military Medical University, Xi'an, China.

CNS Neuroscience & Therapeutics
|January 25, 2023
PubMed
Summary

Postoperative cognitive dysfunction (PND) involves hippocampus-dependent memory deficits. Laparotomy causes PND by increasing NR2B gene methylation, which is reversible with S-adenosylmethionine (SAM) treatment.

Keywords:
DNA methylationNR2BSAMperioperative neurocognitive disorder

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Area of Science:

  • Neuroscience
  • Epigenetics
  • Molecular Biology

Background:

  • Postoperative cognitive dysfunction (PND) is a common complication.
  • NR2B subunit of the NMDA receptor plays a critical role in learning and memory.
  • Epigenetic modifications, such as DNA methylation, are implicated in neurological disorders.

Purpose of the Study:

  • To investigate the role of NR2B in the pathogenesis of PND.
  • To determine the contribution of DNA methylation to NR2B expression in PND.
  • To explore potential therapeutic interventions targeting NR2B methylation.

Main Methods:

  • Adult C57BL/6J mice underwent laparotomy under isoflurane anesthesia.
  • Cognitive function was assessed using the Barnes maze and contextual fear conditioning.
  • NR2B expression, gene methylation, and long-term potentiation (LTP) were analyzed.

Main Results:

  • Laparotomy induced cognitive deficits, reduced NR2B expression, and impaired LTP.
  • NR2B gene hypermethylation was identified as the cause of decreased NR2B expression.
  • S-adenosylmethionine (SAM) administration reversed these effects in a dose-dependent manner.

Conclusions:

  • Laparotomy-induced cognitive decline is mediated by NR2B gene hypermethylation.
  • NR2B epigenetic regulation is a key factor in PND pathogenesis.
  • SAM shows therapeutic potential for PND by modulating NR2B gene methylation.