Gottesman I I, Moldin S O
University of Virginia, Charlottesville 22903, USA.
Clin Genet. 1997 Nov;52(5):404-7. doi: 10.1111/j.1399-0004.1997.tb04361.x.
As the new millennium approaches, research into the genetic aspects of schizophrenia has already made an impressive start toward an integrated model which is discovering roles for genetic agents, environmental agents and experiences, and chance factors. The best model follows that proposed for understanding such complex diseases as coronary artery disease and diabetes. Genetic information has come from both genetic epidemiology and molecular genetics. Evidence for gene regions on 6p and 8p gives the strongest support for harboring schizophrenia susceptibility genes, based on international collaborative studies that "generally" replicate one another; evidence for regions on 3p, 5q, 9p, 20p, and 22q, while less compelling, will encourage focused work. Determining the steps between the regions and the phenotype will challenge the next generation of scientists.
随着新千年的临近，对精神分裂症遗传方面的研究已经朝着一个综合模型取得了令人瞩目的开端，该模型正在揭示遗传因素、环境因素、经历以及偶然因素所起的作用。最佳模型遵循了为理解诸如冠状动脉疾病和糖尿病等复杂疾病而提出的模型。遗传信息来自遗传流行病学和分子遗传学。基于国际合作研究“普遍”相互印证的结果，6p和8p上基因区域的证据为存在精神分裂症易感基因提供了最有力的支持；3p、5q、9p、20p和22q上区域的证据虽然不那么令人信服，但也将激励有针对性的研究工作。确定这些区域与表型之间的步骤将对下一代科学家构成挑战。
