Solís-Añez Ernesto, Delgado-Luengo Wilmer, Hernández María Luisa
Unidad de Genética Médica, Facultad de Medicina, Universidad del Zulia, Maracaibo, Venezuela.
Invest Clin. 2007 Dec;48(4):529-41.
Autism is a complex neurodevelopmental disorder characterized by impairment of social interaction, language, communication, and stereotyped, repetitive behavior. Genetic predisposition to autism has been demonstrated from families and twin studies. Despite recent advances in identifying some susceptibility candidate genes, its underlying neurological mechanism is uncertain. There are genetic, biochemical and neuropathological findings that support the hypothesis that autism could be caused by GABAergic dysfunction and it is partially responsible for the etiology of this disorder. One of the most studied genome regions is the 15q11-q13, where the genes that encode for beta3, alpha5 and gamma3 subunits of the GABAA receptor are located. This review demonstrates evidence that involves this region in autism susceptibility and its likely relation with the hypothesis of GABAergic dysfunction.
自闭症是一种复杂的神经发育障碍,其特征为社交互动、语言、沟通以及刻板重复行为受损。家族研究和双胞胎研究已证实自闭症存在遗传易感性。尽管在确定一些候选易感基因方面取得了最新进展,但其潜在的神经学机制仍不明确。有遗传、生化和神经病理学研究结果支持这样的假说,即自闭症可能由γ-氨基丁酸(GABA)能功能障碍引起,且该功能障碍在一定程度上导致了这种疾病的病因。研究最多的基因组区域之一是15q11-q13,γ-氨基丁酸A(GABAA)受体的β3、α5和γ3亚基的编码基因就位于该区域。这篇综述展示了涉及该区域与自闭症易感性相关的证据,以及它与GABA能功能障碍假说之间可能存在的关系。