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The place of Franz Kallmann's 1938 “the genetics of schizophrenia” in the history of psychiatric genetics
American Journal of Medical Genetics Part B: Neuropsychiatric Genetics ( IF 2.8 ) Pub Date : 2022-01-13 , DOI: 10.1002/ajmg.b.32886
Kenneth S Kendler 1, 2 , Astrid Klee 3
Affiliation  

This essay provides the historical context and key findings of one of the largest fieldwork-based family studies ever done in the history of psychiatric genetics conducted in Berlin by Franz Kallmann from 1929 to 1933. It included over 1,000 schizophrenic probands and 12,500 of their relatives including siblings, offspring, nieces/nephews and grandchildren. The work was analyzed in close collaboration with Rüdin, Schulz, and Luxenburger in Munich. Born of Jewish parents, Kallmann had to leave Germany in 1936, completing and publishing the monograph in the United States in 1938. This study included a number of methodologic advances over the classic 1916 sibling study of Rüdin: (a) joint analysis of multiple classes of relatives; (b) subdivision of schizophrenia into four subtypes; (c) a focus on schizoid personality [schizoidia]; (d) examination of the familial aggregation of schizophrenia; and (e) a more complex genetic model—with schizophrenia arising from a single-recessive gene with 70% penetrance and background polygenic influences, and schizoidia from heterozygotes. Kallmann found important differences in risk of relatives in nuclear versus peripheral subtypes and concluded that schizoidia was a part of schizophrenia disease complex while other psychopathies, feeblemindedness, and organic brain disorders were not. Kallmann was strongly invested in the eugenic implications of his results.

中文翻译:

弗朗茨·卡尔曼 1938 年的《精神分裂症的遗传学》在精神遗传学史上的地位

这篇文章提供了弗朗茨·卡尔曼(Franz Kallmann)从 1929 年到 1933 年在柏林进行的最大的基于实地调查的家庭研究之一的历史背景和主要发现。它包括超过 1,000 名精神分裂症先证者和他们的 12,500 名亲属,包括兄弟姐妹、后代、侄女/侄子和孙子孙女。与 Rüdin、Schulz 和 Luxenburger 在慕尼黑的密切合作对这项工作进行了分析。Kallmann 出生于犹太父母,1936 年不得不离开德国,于 1938 年在美国完成并出版了这本专着。这项研究包括对 1916 年 Rüdin 的经典兄弟姐妹研究的一些方法学进步:(a) 多个班级的联合分析亲属;(b) 将精神分裂症细分为四个亚型;(c) 关注分裂样人格[schizoidia];(d) 检查精神分裂症的家族聚集性;(e) 一个更复杂的遗传模型——精神分裂症是由具有 70% 外显率和背景多基因影响的单隐性基因引起的,而精神分裂症是由杂合子引起的。Kallmann 发现核亚型和外周亚型的亲属风险存在重要差异,并得出结论认为,精神分裂症是精神分裂症综合征的一部分,而其他精神病、弱智和器质性脑疾病则不是。Kallmann 对他的研究结果的优生学意义投入了大量精力。Kallmann 发现核亚型和外周亚型的亲属风险存在重要差异,并得出结论认为,精神分裂症是精神分裂症综合征的一部分,而其他精神病、弱智和器质性脑疾病则不是。Kallmann 对他的研究结果的优生学意义投入了大量精力。Kallmann 发现核亚型和外周亚型的亲属风险存在重要差异,并得出结论认为,精神分裂症是精神分裂症综合征的一部分,而其他精神病、弱智和器质性脑疾病则不是。Kallmann 对他的研究结果的优生学意义投入了大量精力。
更新日期:2022-01-13
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