Cai Na, Verhulst Brad, Andreassen Ole A, Buitelaar Jan, Edenberg Howard J, Hettema John M, Gandal Michael, Grotzinger Andrew, Jonas Katherine, Lee Phil, Mallard Travis T, Mattheisen Manuel, Neale Michael C, Nurnberger John I, Peyrot Wouter J, Tucker-Drob Elliot M, Smoller Jordan W, Kendler Kenneth S
Helmholtz Pioneer Campus, Helmholtz Munich, Neuherberg, Germany.
Computational Health Centre, Helmholtz Munich, Neuherberg, Germany.
Mol Psychiatry. 2025 Apr;30(4):1627-1638. doi: 10.1038/s41380-024-02878-x. Epub 2024 Dec 27.
Psychiatric disorders are highly comorbid, heritable, and genetically correlated [1-4]. The primary objective of cross-disorder psychiatric genetics research is to identify and characterize both the shared genetic factors that contribute to convergent disease etiologies and the unique genetic factors that distinguish between disorders [4, 5]. This information can illuminate the biological mechanisms underlying comorbid presentations of psychopathology, improve nosology and prediction of illness risk and trajectories, and aid the development of more effective and targeted interventions. In this review we discuss how estimates of comorbidity and identification of shared genetic loci between disorders can be influenced by how disorders are measured (phenotypic assessment) and the inclusion or exclusion criteria in individual genetic studies (sample ascertainment). Specifically, the depth of measurement, source of diagnosis, and time frame of disease trajectory have major implications for the clinical validity of the assessed phenotypes. Further, biases introduced in the ascertainment of both cases and controls can inflate or reduce estimates of genetic correlations. The impact of these design choices may have important implications for large meta-analyses of cohorts from diverse populations that use different forms of assessment and inclusion criteria, and subsequent cross-disorder analyses thereof. We review how assessment and ascertainment affect genetic findings in both univariate and multivariate analyses and conclude with recommendations for addressing them in future research.
精神疾病具有高度的共病性、遗传性和基因相关性[1-4]。跨疾病精神遗传学研究的主要目标是识别并表征促成疾病病因趋同的共同遗传因素以及区分不同疾病的独特遗传因素[4,5]。这些信息能够阐明精神病理学共病表现背后的生物学机制,改善疾病分类学以及疾病风险和病程的预测,并有助于开发更有效、更具针对性的干预措施。在本综述中,我们将讨论疾病的测量方式(表型评估)以及个体基因研究中的纳入或排除标准(样本确定)如何影响共病估计和疾病间共享基因座的识别。具体而言,测量深度、诊断来源和疾病病程的时间框架对所评估表型的临床有效性具有重要影响。此外,病例和对照确定过程中引入的偏差可能会夸大或降低基因相关性估计。这些设计选择的影响可能对来自不同人群、使用不同评估形式和纳入标准的队列进行的大型荟萃分析及其后续的跨疾病分析具有重要意义。我们将综述评估和确定过程如何在单变量和多变量分析中影响基因研究结果,并在结尾给出在未来研究中解决这些问题的建议。