Department of Biotechnology, Baba Ghulam Shah Badshah University, Rajouri, J&K, 185234, India.
Department of Genetics, Yale School of Medicine, New Haven, CT, USA.
Mol Biol Rep. 2021 Feb;48(2):1607-1614. doi: 10.1007/s11033-021-06166-7. Epub 2021 Feb 2.
Giant axonal neuropathy (GAN) is a severe and rare autosomal recessive neurodegenerative disorder of childhood affecting both the peripheral and central nervous systems (CNS). It is caused by mutations in the GAN (gigaxonin) gene linked to chromosome 16q24. Here, we present a 15-year-old male patient with GAN from a consanguineous family of Poonch, Jammu and Kashmir (J&K)-India. Whole-exome sequencing (WES) was employed to unravel the genetic cause of GAN in the proband. Pathogenic variant identified with WES was confirmed in other affected sibling using Sanger sequencing. Magnetic resonance imaging (MRI) and detailed clinical investigation was also carried out on proband. WES revealed a novel homozygous stopgain GAN mutation (NM_022041, c.C1028G, p.S343X) in the patient. MRI of brain displayed bilateral symmetrical confluent areas of deep white matter signal changes affecting periventricular regions (with sparing of subcortical U-fibers), posterior limbs of internal capsules, thalami, external capsules, and semioval centers. The patient was initially suspected to be a case of metachromatic leukodystrophy. However, WES analysis revealed a pathogenic variant in GAN gene as causative. No other pathogenic variant relevant to any other type of dystrophy was reported in WES. Our findings extend the geographical distribution of GAN to even a very remote region in India, extend the mutational and imaging spectrum of GAN and substantiate the need for introducing genetic testing and counselling in primary referral centers/district hospitals in India.
巨轴索神经病(GAN)是一种严重且罕见的常染色体隐性儿童神经退行性疾病,影响外周和中枢神经系统(CNS)。它是由染色体 16q24 上的 GAN(巨轴索蛋白)基因突变引起的。在这里,我们介绍了来自印度查谟和克什米尔(J&K)蓬奇的一个近亲家庭的 15 岁男性 GAN 患者。全外显子组测序(WES)用于揭示先证者 GAN 的遗传原因。使用 Sanger 测序在其他受影响的兄弟姐妹中证实了 WES 鉴定出的致病性变异。还对先证者进行了磁共振成像(MRI)和详细的临床检查。WES 显示患者存在一种新的纯合性移码 GAN 突变(NM_022041,c.C1028G,p.S343X)。大脑 MRI 显示双侧对称融合的深部白质信号变化,影响脑室周围区域(皮质下 U 纤维不受累)、内囊后肢、丘脑、外囊和半卵圆中心。该患者最初被怀疑为脑硫脂沉积病,但 WES 分析显示 GAN 基因中的致病性变异是致病原因。WES 未报告与任何其他类型的营养不良相关的其他致病性变异。我们的发现将 GAN 的地理分布扩展到印度的一个非常偏远的地区,扩展了 GAN 的突变和成像谱,并证实了在印度的初级转诊中心/地区医院引入基因检测和咨询的必要性。