问题性酒精使用和焦虑障碍的共享遗传架构和神经生物学途径
Mingjian Shi1,2, Tommy Gunawan1,2, Samantha G Malone1,2
1Department of Medical and Clinical Psychology, Uniformed Services University, Bethesda, MD, 20814, US.
medRxiv : the preprint server for health sciences
|December 8, 2025
概括
问题性酒精使用和焦虑症有着重要的遗传联系和因果关系. 这些发现揭示了重叠的神经生物学途径,有助于两种情况.
科学领域:
- 遗传学 是一个遗传学.
- 神经生物学 神经生物学 神经生物学
- 精神病学是一个精神病学.
背景情况:
- 问题性酒精使用 (PAU) 和焦虑障碍 (ANX) 经常同时发生,这表明它们有共同的遗传和神经生物学基础.
- 正确的因果方向性和驱动这种重叠的机制在很大程度上仍未确定.
研究的目的:
- 研究PAU和ANX之间共享的遗传架构和神经生物学途径.
- 阐明双向因果关系,并确定特定的遗传位置和基因表达模式,涉及到它们的共同发生.
主要方法:
- 使用全基因组关联研究 (GWAS) 对PAU和ANX的总结统计数据.
- 采用孟德尔的随机化,MiXeR,局部分析 (co) 变体关联,并联虚假发现率 (conjFDR) 来分析遗传重叠.
- 使用FUMA绘制基因位置,在多种组织类型中进行差异性基因表达分析,并使用人类大脑细胞图谱分析细胞类型特异性.
主要成果:
- 门德尔随机化表明ANX和PAU之间的双向因果关系.
- 确定了中度的多基因重叠 (52.5%) 和遗传相关性 (r_g = 0.44),通过conjFDR识别了97个共享的单核酸多态 (SNP).
- 发现大脑区域的丰富基因表达,包括前额叶皮质,海马和杏仁体,在神经元中具有特定的丰富.
结论:
- 确认了PAU和ANX之间的大量遗传和神经生物学重叠.
- 突出了这些疾病之间的相互,因果关系,由共享的遗传变异和相关大脑区域的差异性基因表达支持.
- 这些发现强调了共同的潜在因果机制,将问题性酒精使用与焦虑障碍联系起来.
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