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[肌张力障碍的遗传学]

[Genetics of dystonia].

作者信息

Klein C, Kann M, Kis B, Pramstaller P P, Breakefield X O, Ozelius L J, Vieregge P

机构信息

Neurology Department, Massachusetts General Hospital, Boston, USA.

出版信息

Nervenarzt. 2000 Jun;71(6):431-41. doi: 10.1007/s001150050604.

Abstract

To date, at least 12 types of primary dystonia can be distinguished on a genetic basis. A 3-bp deletion in the DYT1 gene causes early onset, generalized torsion dystonia (TD), and mutations in the GTP cyclohydrolase I and the tyrosine hydroxylase genes result in dopa-responsive dystonia (DYT5). A missense change in the D2 dopamine receptor in one large family (DYT11) has recently been implicated in myoclonus-dystonia. Furthermore, seven other loci for dystonia genes have been mapped to chromosomal regions, including a locus for a mixed dystonia phenotype (DYT6), one form of focal dystonia (DYT7), three types of paroxysmal dystonia (DYT8-10), X-linked dystonia-parkinsonism (DYT3), and rapid-onset dystonia-parkinsonism (DYT12). No positive linkage results have yet been obtained for autosomal recessive TD (DYT2) and several other families of different types of dominantly inherited TD (DYT4). In addition, hereditary secondary dystonia may occur as part of familial diseases of the basal ganglia, metabolic and storage disorders, and various X-linked and other familial neurodegenerative syndromes affecting the basal ganglia. It may be anticipated that the traditional clinical and etiological classifications of dystonia will increasingly be replaced by a genetic one and that the identification of more dystonia genes may lead to a better understanding of these largely nondegenerative disorders.

摘要

迄今为止,至少有12种原发性肌张力障碍可在基因基础上加以区分。DYT1基因中的一个3碱基对缺失会导致早发性全身性扭转性肌张力障碍(TD),而GTP环化水解酶I和酪氨酸羟化酶基因的突变会导致多巴反应性肌张力障碍(DYT5)。最近发现,在一个大家族中(DYT11),D2多巴胺受体的错义变化与肌阵挛性肌张力障碍有关。此外,肌张力障碍基因的其他七个位点已被定位到染色体区域,包括一种混合型肌张力障碍表型的位点(DYT6)、一种局限性肌张力障碍(DYT7)、三种阵发性肌张力障碍(DYT8 - 10)、X连锁肌张力障碍-帕金森综合征(DYT3)以及快速起病的肌张力障碍-帕金森综合征(DYT12)。对于常染色体隐性TD(DYT2)以及其他几个不同类型的显性遗传性TD家族(DYT4),尚未获得阳性连锁结果。此外,遗传性继发性肌张力障碍可能作为基底神经节家族性疾病、代谢和储存障碍以及各种影响基底神经节的X连锁和其他家族性神经退行性综合征的一部分出现。可以预期,肌张力障碍传统的临床和病因学分类将越来越多地被基因分类所取代,而且更多肌张力障碍基因的鉴定可能会使人们对这些基本上非退行性疾病有更好的理解。

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