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青少年双相情感障碍的家族、双胞胎、收养及分子遗传学研究。

Family, twin, adoption, and molecular genetic studies of juvenile bipolar disorder.

作者信息

Althoff Robert R, Faraone Stephen V, Rettew David C, Morley Christopher P, Hudziak James J

机构信息

Department of Psychiatry, Massachusetts General Hospital, Boston, MA, USA.

出版信息

Bipolar Disord. 2005 Dec;7(6):598-609. doi: 10.1111/j.1399-5618.2005.00268.x.

Abstract

Juvenile bipolar disorder (JBD) has been a subject of significant research and debate. Phenotypic differences between JBD and adult-onset bipolar disorder have led researchers to question whether or not similar neuropathologic mechanisms will be found. While much is known about the genetic and environmental contributions to the adult-onset phenotype, less is known about their contributions to JBD. Here, we review family, twin, adoption, and molecular genetic studies of JBD. Behavioral genetic data suggest both genetic and environmental contributions to JBD, while molecular genetic studies find linkage to age of onset of bipolar disorder to chromosomes 12p, 14q, and 15q. Additionally, changes associated with symptom age of onset have been recently reported in the brain-derived neurotrophic factor (BDNF) and glycogen synthase kinase 3-beta (GSK3-beta) genes. We contend that further progress in discovering the precise genetic and environmental contributions to JBD may depend on advances in phenotypic refinement, an increased appreciation of comorbid conditions, and more investigation of the longitudinal course of the disorder.

摘要

青少年双相情感障碍(JBD)一直是大量研究和辩论的主题。JBD与成人期双相情感障碍之间的表型差异促使研究人员质疑是否会发现相似的神经病理机制。虽然对于成人期双相情感障碍的遗传和环境因素贡献已有很多了解,但对于它们对JBD的贡献却知之甚少。在此,我们综述了JBD的家系、双生子、收养及分子遗传学研究。行为遗传学数据表明遗传和环境因素均对JBD有影响,而分子遗传学研究发现双相情感障碍的发病年龄与12号染色体短臂、14号染色体长臂和15号染色体长臂存在连锁关系。此外,最近有报道称脑源性神经营养因子(BDNF)和糖原合酶激酶3β(GSK3β)基因出现了与症状发病年龄相关的变化。我们认为,在发现JBD的确切遗传和环境因素贡献方面取得进一步进展可能取决于表型细化方面的进展、对共病情况的更多认识以及对该疾病纵向病程的更多研究。

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