Department of Psychiatry, Fujita Health University School of Medicine, Toyoake, Japan.
Laboratory for Statistical Analysis, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
Schizophr Bull. 2019 Jun 18;45(4):824-834. doi: 10.1093/schbul/sby140.
Genome-wide association studies (GWASs) have identified >100 susceptibility loci for schizophrenia (SCZ) and demonstrated that SCZ is a polygenic disorder determined by numerous genetic variants but with small effect size. We conducted a GWAS in the Japanese (JPN) population (a) to detect novel SCZ-susceptibility genes and (b) to examine the shared genetic risk of SCZ across (East Asian [EAS] and European [EUR]) populations and/or that of trans-diseases (SCZ, bipolar disorder [BD], and major depressive disorder [MDD]) within EAS and between EAS and EUR (trans-diseases/populations). Among the discovery GWAS subjects (JPN-SCZ GWAS: 1940 SCZ cases and 7408 controls) and replication dataset (4071 SCZ cases and 54479 controls), both comprising JPN populations, 3 novel susceptibility loci for SCZ were identified: SPHKAP (Pbest = 4.1 × 10-10), SLC38A3 (Pbest = 5.7 × 10-10), and CABP1-ACADS (Pbest = 9.8 × 10-9). Subsequent meta-analysis between our samples and those of the Psychiatric GWAS Consortium (PGC; EUR samples) and another study detected 12 additional susceptibility loci. Polygenic risk score (PRS) prediction revealed a shared genetic risk of SCZ across populations (Pbest = 4.0 × 10-11) and between SCZ and BD in the JPN population (P ~ 10-40); however, a lower variance-explained was noted between JPN-SCZ GWAS and PGC-BD or MDD within/across populations. Genetic correlation analysis supported the PRS results; the genetic correlation between JPN-SCZ and PGC-SCZ was ρ = 0.58, whereas a similar/lower correlation was observed between the trans-diseases (JPN-SCZ vs JPN-BD/EAS-MDD, rg = 0.56/0.29) or trans-diseases/populations (JPN-SCZ vs PGC-BD/MDD, ρ = 0.38/0.12). In conclusion, (a) Fifteen novel loci are possible susceptibility genes for SCZ and (b) SCZ "risk" effect is shared with other psychiatric disorders even across populations.
全基因组关联研究(GWAS)已经确定了超过 100 个精神分裂症(SCZ)易感基因,并表明 SCZ 是一种由许多遗传变异决定的多基因疾病,但效应大小较小。我们在日本(JPN)人群中进行了 GWAS,以检测新的 SCZ 易感基因,并检查 SCZ 在(东亚 [EAS] 和欧洲 [EUR])人群中的共享遗传风险,或 EAS 内的跨疾病(SCZ、双相情感障碍 [BD] 和重度抑郁症 [MDD])和 EAS 与 EUR 之间的跨疾病/人群(跨疾病/人群)的遗传风险。在发现 GWAS 受试者(JPN-SCZ GWAS:1940 例 SCZ 病例和 7408 例对照)和复制数据集(4071 例 SCZ 病例和 54479 例对照)中,这两个数据集均包含 JPN 人群,确定了 3 个新的 SCZ 易感基因:SPHKAP(Pbest = 4.1×10-10)、SLC38A3(Pbest = 5.7×10-10)和 CABP1-ACADS(Pbest = 9.8×10-9)。在我们的样本与精神疾病 GWAS 联盟(PGC;EUR 样本)和另一项研究的样本之间进行的后续荟萃分析中,检测到了另外 12 个易感基因。多基因风险评分(PRS)预测显示,SCZ 在人群之间存在共享的遗传风险(Pbest = 4.0×10-11),在 JPN 人群中,SCZ 与 BD 之间存在遗传风险(P~10-40);然而,在 JPN-SCZ GWAS 与 PGC-BD 或 MDD 之间,人群内/人群之间的解释方差较低。遗传相关性分析支持 PRS 结果;JPN-SCZ 和 PGC-SCZ 之间的遗传相关性为 ρ=0.58,而在跨疾病(JPN-SCZ 与 JPN-BD/EAS-MDD,rg=0.56/0.29)或跨疾病/人群(JPN-SCZ 与 PGC-BD/MDD,ρ=0.38/0.12)之间观察到类似/较低的相关性。总之,(a)15 个新的基因座可能是 SCZ 的易感基因,(b)SCZ“风险”效应在人群之间甚至与其他精神疾病共享。