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Background <p>MicroRNAs are critical regulators of neuronal plasticity, synaptic signaling, and stress response, and their dysregulation has been implicated in substance use disorders. However, postmortem evidence on their involvement in Alcohol Use Disorder (AUD) remains limited. We aimed to investigate the expression patterns of miR-132, miR-133b, miR-140, miR-181a, miR-190, and miR-212 in the prefrontal cortex of individuals with AUD.</p> Methods <p>Prefrontal cortex tissues were obtained postmortem from 30 individuals with documented AUD and 30 age- and sex-matched non-alcohol users. Total RNA was isolated, reverse-transcribed into cDNA, and analyzed by quantitative real-time PCR. Relative expression levels were calculated using the 2<sup>−ΔΔCT</sup> method, with U6 RNA as endogenous control.</p> Results <p>Individuals with AUD exhibited increased expression of miR-133b (fold change: 4.4, <i>p</i> = 0.035), and miR-212 (fold change: 1.57, <i>p</i> = 0.006), while miR-132 (fold change: 3, <i>p</i> &lt; 0.001) and miR-190 (fold change: 2.63, <i>p</i> = 0.003) were markedly downregulated compared with controls.</p> Conclusions <p>The differential expression of these miRNAs suggests their involvement in neuronal signaling pathways underlying AUD, particularly those linked to synaptic plasticity and stress-related transcriptional regulation.</p>

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Altered microRNA expression profiles in the postmortem prefrontal cortex of individuals with alcohol use disorder: a case–control study

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月29日

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  • Burcu Çaykara Peran,
  • Hani Alsaadoni,
  • Mehmet Zahit Çıracı,
  • Sibel Kuraş,
  • Halime Hanım Pençe,
  • Yalçın Büyük,
  • Bekir Erdoğan,
  • Sadrettin Pençe

摘要

Background

MicroRNAs are critical regulators of neuronal plasticity, synaptic signaling, and stress response, and their dysregulation has been implicated in substance use disorders. However, postmortem evidence on their involvement in Alcohol Use Disorder (AUD) remains limited. We aimed to investigate the expression patterns of miR-132, miR-133b, miR-140, miR-181a, miR-190, and miR-212 in the prefrontal cortex of individuals with AUD.

Methods

Prefrontal cortex tissues were obtained postmortem from 30 individuals with documented AUD and 30 age- and sex-matched non-alcohol users. Total RNA was isolated, reverse-transcribed into cDNA, and analyzed by quantitative real-time PCR. Relative expression levels were calculated using the 2−ΔΔCT method, with U6 RNA as endogenous control.

Results

Individuals with AUD exhibited increased expression of miR-133b (fold change: 4.4, p = 0.035), and miR-212 (fold change: 1.57, p = 0.006), while miR-132 (fold change: 3, p < 0.001) and miR-190 (fold change: 2.63, p = 0.003) were markedly downregulated compared with controls.

Conclusions

The differential expression of these miRNAs suggests their involvement in neuronal signaling pathways underlying AUD, particularly those linked to synaptic plasticity and stress-related transcriptional regulation.