Horváth Rita, Reilmann Ralf, Holinski-Feder Elke, Ringelstein E Bernd, Klopstock Thomas
Friedrich-Baur-Institute, Department of Neurology, Ludwig-Maximilians-University, Munich, Ziemssenstr. 1, 80336 Munich, Germany.
Neuromuscul Disord. 2008 Jul;18(7):553-6. doi: 10.1016/j.nmd.2008.05.002. Epub 2008 Jun 30.
While Mitochondrial Encephalomyopathy, Lactic Acidosis, and Stroke-like episodes (MELAS) is typically associated with mutations in the mitochondrial tRNA(Leu) gene, mutations in complex I subunit genes of the mtDNA have emerged as a second significant cause. Here we report a novel mutation in the mitochondrial complex I subunit gene ND1 in a patient with late-onset MELAS. The 3380G>A mutation shows very good evidence of pathogenicity as it is heteroplasmic, undetectable in controls, alters a highly conserved amino acid, and is more abundant in ragged-red than in normal muscle fibers. These findings support the significant role of complex I mutations in MELAS.
虽然线粒体脑肌病伴乳酸血症和卒中样发作(MELAS)通常与线粒体tRNA(Leu)基因突变相关,但线粒体DNA复合体I亚基基因突变已成为第二个重要病因。在此,我们报告一例迟发性MELAS患者线粒体复合体I亚基基因ND1中的一个新突变。3380G>A突变具有很强的致病性证据,因为它是异质性的,在对照中未检测到,改变了一个高度保守的氨基酸,并且在破碎红肌纤维中的含量高于正常肌纤维。这些发现支持了复合体I突变在MELAS中的重要作用。