Torisu Hiroyuki, Iwaki Akiko, Takeshita Kenzo, Hiwatashi Akio, Sanefuji Masafumi, Fukumaki Yasuyuki, Hara Toshiro
Department of Pediatrics, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Brain Dev. 2012 Nov;34(10):852-6. doi: 10.1016/j.braindev.2012.02.006. Epub 2012 Mar 7.
We report herein a case of 2-year-old boy diagnosed with a mild form of Pelizaeus-Merzbacher disease due to deletion of the entire proteolipid protein 1 (PLP1) gene. The patient demonstrated spastic quadriplegia, mental retardation, and microcephaly. He exhibited brainstem auditory evoked potentials with prolonged interpeak latencies and magnetic resonance imaging characteristics suggestive of hypomyelination in most areas of the brain with the exception of the brainstem, cerebellar peduncles, corpus callosum, and the posterior limbs of the internal capsules. Proton magnetic resonance spectroscopy revealed a mildly reduced ratio of N-acetyl aspartate to creatine levels in the white matter, suggesting axonal involvement. Additionally, nerve conduction velocity of the lower extremities was mildly decreased. Genetic analysis showed a deletion of PLP1 in this patient. Further genome mapping followed by sequence analysis of the deletion breakpoints revealed that a genomic region, about 73 kb in length, including the entire PLP1 and RAB9B, was deleted. The size of the deletion was the smallest among those previously reported in this region. Except for the 1-base pair microhomology, there were no homologous sequences between the regions around the distal and proximal breakpoints, which suggests that the deletion occurred by nonhomologous end joining.
我们在此报告一例2岁男孩,因整个蛋白脂蛋白1(PLP1)基因缺失而被诊断为轻度佩利措伊斯-梅茨巴赫病。该患者表现为痉挛性四肢瘫痪、智力发育迟缓及小头畸形。他的脑干听觉诱发电位显示峰间期延长,磁共振成像特征提示除脑干、小脑脚、胼胝体及内囊后肢外,大脑大部分区域存在髓鞘形成不良。质子磁共振波谱显示白质中N-乙酰天门冬氨酸与肌酸水平的比值略有降低,提示轴突受累。此外,下肢神经传导速度略有下降。基因分析显示该患者存在PLP1基因缺失。进一步的基因组定位及缺失断点的序列分析表明,一个长度约73 kb的基因组区域被删除,该区域包括整个PLP1和RAB9B基因。此次缺失的大小是该区域此前报道中最小的。除了1个碱基对的微同源性外,远端和近端断点周围区域之间没有同源序列,这表明该缺失是通过非同源末端连接发生的。