Ewald H, Mors O, Friedrich U, Flint T, Kruse T
Institute of Basic Psychiatric Research, Psychiatric Hospital in Aarhus, Denmark.
Psychiatr Genet. 1994 Spring;4(1):13-22. doi: 10.1097/00041444-199421000-00003.
Mutations at the tyrosine hydroxylase or dopamine D2 receptor loci causing manic depressive illness are unlikely in two families reported here. Linkage was excluded for both loci assuming a dominant mode of transmission and for the tyrosine hydroxylase locus also assuming a recessive mode of transmission. The exclusion was significant using models based on severity of psychopathology and a model requiring severe illness also in first-degree relatives. Conservative genetic parameters were used to minimize misclassification.
本文报道的两个家族中，不太可能存在酪氨酸羟化酶或多巴胺D2受体基因座的突变导致躁郁症。假设为显性遗传模式，两个基因座均排除了连锁关系；假设为隐性遗传模式，酪氨酸羟化酶基因座也排除了连锁关系。使用基于精神病理学严重程度的模型以及要求一级亲属也患有严重疾病的模型，排除结果具有显著性。使用保守的遗传参数以尽量减少错误分类。
