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Background <p>DNA methylation may play a regulatory role in delirium, a multifactorial neuropsychiatric syndrome that arises from interactions between predisposing vulnerabilities (e.g., aging, neurodegeneration) and acute precipitating factors (e.g., inflammation, surgery, critical illness). The purpose of this systematic review is to critically assess the evidence supporting the role of DNA methylation in biological processes associated with delirium.</p> Results <p>Of 1,110 articles identified, nine studies met our inclusion criteria. Six studies examined differential DNA methylation at candidate CpG sites, while three assessed age-related methylation patterns stratified by delirium. Among the four studies that performed genome-wide differential methylation analysis, two independent studies identified two different CpG sites (cg21295729 – <i>LDLRAD4</i> (43 cases vs. 44 controls; blood), cg16526133 – <i>ADAMTS9</i> (11cases vs. 25 controls; brain) that were hypomethylated in patients with delirium, whereas the remaining two studies did not find statistically significant differences. Gene specific analysis of methylation levels of CpG sites annotated to <i>TNF</i> showed a negative correlation with age in PBMCs and whole blood of delirious patients, but not in saliva, buccal or control samples. A positive correlation with age was observed for sites annotated to neurotrophic signaling genes (<i>BDNF</i>,<i> GDNF</i>,<i> NR4A2</i>).</p> Conclusions <p>This review highlights that, despite a strong theoretical rationale suggesting that DNA methylation may contribute to the development of delirium, robust evidence remains lacking. Existing studies are limited both in number and in methodological rigor, constraining firm conclusions.</p>

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A systematic review on the contribution of DNA methylation to delirium pathophysiology

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月20日

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  • Jim Jacob,
  • Maria Zernova,
  • Inge M. Strating,
  • Barbara van Munster,
  • Federica Sarno,
  • Monika Trzpis

摘要

Background

DNA methylation may play a regulatory role in delirium, a multifactorial neuropsychiatric syndrome that arises from interactions between predisposing vulnerabilities (e.g., aging, neurodegeneration) and acute precipitating factors (e.g., inflammation, surgery, critical illness). The purpose of this systematic review is to critically assess the evidence supporting the role of DNA methylation in biological processes associated with delirium.

Results

Of 1,110 articles identified, nine studies met our inclusion criteria. Six studies examined differential DNA methylation at candidate CpG sites, while three assessed age-related methylation patterns stratified by delirium. Among the four studies that performed genome-wide differential methylation analysis, two independent studies identified two different CpG sites (cg21295729 – LDLRAD4 (43 cases vs. 44 controls; blood), cg16526133 – ADAMTS9 (11cases vs. 25 controls; brain) that were hypomethylated in patients with delirium, whereas the remaining two studies did not find statistically significant differences. Gene specific analysis of methylation levels of CpG sites annotated to TNF showed a negative correlation with age in PBMCs and whole blood of delirious patients, but not in saliva, buccal or control samples. A positive correlation with age was observed for sites annotated to neurotrophic signaling genes (BDNF, GDNF, NR4A2).

Conclusions

This review highlights that, despite a strong theoretical rationale suggesting that DNA methylation may contribute to the development of delirium, robust evidence remains lacking. Existing studies are limited both in number and in methodological rigor, constraining firm conclusions.