Mutoh T, Sobue I, Naoi M, Matsuoka Y, Kiuchi K, Sugimura K
Neurology. 1986 Jan;36(1):54-9. doi: 10.1212/wnl.36.1.54.
Three adult patients in a single family showed severe myoclonus, ataxia, and pyramidal signs. Enzymatic analysis of lymphocytes, plasma, and cultured skin fibroblasts showed marked deficiency of beta-galactosidase activity, more profound with GM1 ganglioside than with another natural substrate, asialofetuin. Other lysosomal hydrolases were normal. Although the physical signs were similar to those of types 1 and 2 GM1 gangliosidosis, none had bony abnormalities.
一个家族中的三名成年患者表现出严重的肌阵挛、共济失调和锥体束征。对淋巴细胞、血浆和培养的皮肤成纤维细胞进行酶分析显示,β-半乳糖苷酶活性明显缺乏,与GM1神经节苷脂相比,对另一种天然底物脱唾液酸胎球蛋白的缺乏更为严重。其他溶酶体水解酶正常。尽管体征与1型和2型GM1神经节苷脂贮积症相似,但无一例有骨骼异常。