1 Institut Cochin, Université Paris-Descartes, CNRS (UMR 8104), Paris, France2 Inserm, U1016, Paris, France3 Université Paris Descartes, Sorbonne Paris Cité, Institut Imagine, Paris, France4 INSERM UMR-1163, Embryology and genetics of congenital malformations, Paris, France5 Service de Neurologie pédiatrique, Assistance Publique-Hôpitaux de Paris (AP-HP), hôpital Necker, Paris, France
1 Institut Cochin, Université Paris-Descartes, CNRS (UMR 8104), Paris, France2 Inserm, U1016, Paris, France.
Brain. 2014 Jun;137(Pt 6):1676-700. doi: 10.1093/brain/awu082.
Complex cortical malformations associated with mutations in tubulin genes: TUBA1A, TUBA8, TUBB2B, TUBB3, TUBB5 and TUBG1 commonly referred to as tubulinopathies, are a heterogeneous group of conditions with a wide spectrum of clinical severity. Among the 106 patients selected as having complex cortical malformations, 45 were found to carry mutations in TUBA1A (42.5%), 18 in TUBB2B (16.9%), 11 in TUBB3 (10.4%), three in TUBB5 (2.8%), and three in TUBG1 (2.8%). No mutations were identified in TUBA8. Systematic review of patients' neuroimaging and neuropathological data allowed us to distinguish at least five cortical malformation syndromes: (i) microlissencephaly (n = 12); (ii) lissencephaly (n = 19); (iii) central pachygyria and polymicrogyria-like cortical dysplasia (n = 24); (iv) generalized polymicrogyria-like cortical dysplasia (n = 6); and (v) a 'simplified' gyral pattern with area of focal polymicrogyria (n = 19). Dysmorphic basal ganglia are the hallmark of tubulinopathies (found in 75% of cases) and are present in 100% of central pachygyria and polymicrogyria-like cortical dysplasia and simplified gyral malformation syndromes. Tubulinopathies are also characterized by a high prevalence of corpus callosum agenesis (32/80; 40%), and mild to severe cerebellar hypoplasia and dysplasia (63/80; 78.7%). Foetal cases (n = 25) represent the severe end of the spectrum and show specific abnormalities that provide insights into the underlying pathophysiology. The overall complexity of tubulinopathies reflects the pleiotropic effects of tubulins and their specific spatio-temporal profiles of expression. In line with previous reports, this large cohort further clarifies overlapping phenotypes between tubulinopathies and although current structural data do not allow prediction of mutation-related phenotypes, within each mutated gene there is an associated predominant pattern of cortical dysgenesis allowing some phenotype-genotype correlation. The core phenotype of TUBA1A and TUBG1 tubulinopathies are lissencephalies and microlissencephalies, whereas TUBB2B tubulinopathies show in the majority, centrally predominant polymicrogyria-like cortical dysplasia. By contrast, TUBB3 and TUBB5 mutations cause milder malformations with focal or multifocal polymicrogyria-like cortical dysplasia with abnormal and simplified gyral pattern.
与微管蛋白基因(TUBA1A、TUBA8、TUBB2B、TUBB3、TUBB5 和 TUBG1)突变相关的复杂皮质发育不良:通常称为微管蛋白病,是一组具有广泛临床严重程度的异质性疾病。在被选为具有复杂皮质发育不良的 106 名患者中,发现 45 名患者携带 TUBA1A 突变(42.5%),18 名患者携带 TUBB2B 突变(16.9%),11 名患者携带 TUBB3 突变(10.4%),3 名患者携带 TUBB5 突变(2.8%),3 名患者携带 TUBG1 突变(2.8%)。TUBA8 中未发现突变。对患者神经影像学和神经病理学数据的系统回顾使我们能够区分至少五种皮质发育不良综合征:(i)微脑裂畸形(n=12);(ii)无脑回畸形(n=19);(iii)中央脑回发育不良和多微脑回样皮质发育不良(n=24);(iv)弥漫性多微脑回样皮质发育不良(n=6);和(v)“简化”脑回模式伴局灶性多微脑回(n=19)。基底节畸形是微管蛋白病的特征(在 75%的病例中发现),存在于 100%的中央脑回发育不良和多微脑回样皮质发育不良以及简化脑回畸形综合征中。微管蛋白病还表现为胼胝体发育不全的高患病率(32/80;40%),以及轻度至重度小脑发育不良和畸形(63/80;78.7%)。胎儿病例(n=25)代表了该谱的严重端,显示出特定的异常,为潜在的病理生理学提供了见解。微管蛋白病的总体复杂性反映了微管蛋白的多效性及其特定的时空表达谱。与之前的报告一致,这个大型队列进一步阐明了微管蛋白病之间重叠的表型,尽管目前的结构数据不允许预测与突变相关的表型,但在每个突变基因中,都存在与皮质发育不良相关的主要模式,从而允许进行一些表型-基因型相关性分析。TUBA1A 和 TUBG1 微管蛋白病的核心表型是无脑回畸形和微脑回畸形,而 TUBB2B 微管蛋白病主要表现为中央多微脑回样皮质发育不良。相比之下,TUBB3 和 TUBB5 突变导致局灶性或多灶性多微脑回样皮质发育不良伴异常和简化脑回模式的轻度畸形。