酒精使用障碍和身体质量指数显示出遗传形和共享的神经关联
Samantha G Malone1,2, Christal N Davis3,4, Zachary Piserchia1,2
1Uniformed Services University of the Health Sciences, Department of Medical and Clinical Psychology, Bethesda, MD 20814, United States.
medRxiv : the preprint server for health sciences
|May 15, 2024
概括
酒精使用障碍 (AUD) 和体重指数 (BMI) 具有显著的多基因重叠,尽管遗传相关性很小. 与奖励和执行功能相关的大脑区域的对立变异效应解释了这一发现.
科学领域:
- 遗传学和神经生物学
- 代谢和行为健康
背景情况:
- 酒精使用障碍 (AUD) 和体重指数 (BMI) 分享神经生物学途径.
- 在AUD和BMI之间的最小遗传相关性 (rg) 表明复杂的遗传相互作用,可能是由于对立的变异效应.
研究的目的:
- 为了研究AUD和BMI之间共享的遗传结构.
- 识别共享的基因位置及其定向效应.
- 探索AUD和BMI之间的关系的神经生物学基础.
主要方法:
- 应用MiXeR用于多基因重叠分析.
- 利用结合错误发现率 (conjFDR) 来检测共享的位置和定向效应.
- 使用 (共) 变体协会 (LAVA),FUMA,GTEx和BrainX的局部分析可以进行全面的遗传和功能分析.
主要成果:
- 尽管整体遗传相关性较低 (rg = -0.03),但MiXeR发现了大量的多基因重叠 (82.2%) .
- 确定了132个共享的领先SNP,包括53个新型SNP,具有一致和不一致的效果.
- 组织丰富分析显示在大脑区域表达,杏仁体和尾状核体积与AUD和BMI有关.
结论:
- 相反的遗传变异效应解释了AUD和BMI之间的低遗传相关性.
- 共享基因架构涉及对执行功能和奖励处理至关重要的大脑区域.
- 澄清了AUD和BMI之间的多基因重叠和神经生物学机制.
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