Weihl Conrad C, Baloh Robert H, Lee Youjin, Chou Tsui-Fen, Pittman Sara K, Lopate Glenn, Allred Peggy, Jockel-Balsarotti Jennifer, Pestronk Alan, Harms Matthew B
Department of Neurology, Hope Center for Neurologic Disorders, Washington University School of Medicine, Saint Louis, MO 63110, United States.
Department of Neurology, Regenerative Medicine Institute, Cedars-Sinai Medical Center, 8730 Alden Drive, Los Angeles, CA 90048, United States.
Neuromuscul Disord. 2015 Apr;25(4):289-96. doi: 10.1016/j.nmd.2014.12.009. Epub 2015 Jan 6.
Sporadic inclusion body myositis (sIBM) has clinical, pathologic and pathomechanistic overlap with some inherited muscle and neurodegenerative disorders. In this study, DNA from 79 patients with sIBM was collected and the sequencing of 38 genes associated with hereditary inclusion body myopathy (IBM), myofibrillar myopathy, Emery-Dreifuss muscular dystrophy, distal myopathy, amyotrophic lateral sclerosis and dementia along with C9orf72 hexanucleotide repeat analysis was performed. No C9orf72 repeat expansions were identified, but; 27 rare (minor allele frequency <1%) missense coding variants in several other genes were identified. One patient carried a p.R95C missense mutation in VCP and another carried a previously reported p.I27V missense mutation in VCP. Mutations in VCP cause IBM associated with Paget's disease of the bone (PDB) and fronto-temporal dementia (IBMPFD). Neither patient had a family history of weakness or manifested other symptoms reported with VCP mutations such as PDB or dementia. In vitro analysis of these VCP variants found that they both disrupted autophagy similar to other pathogenic mutations. Although no clear genetic etiology has been implicated in sIBM pathogenesis, our study suggests that genetic evaluation in sIBM may be clinically meaningful and lend insight into its pathomechanism.
散发性包涵体肌炎(sIBM)在临床、病理及发病机制上与某些遗传性肌肉和神经退行性疾病存在重叠。在本研究中,收集了79例sIBM患者的DNA,并对38个与遗传性包涵体肌病(IBM)、肌原纤维肌病、埃默里-德赖富斯肌营养不良症、远端肌病、肌萎缩侧索硬化症和痴呆相关的基因进行了测序,同时进行了C9orf72六核苷酸重复序列分析。未发现C9orf72重复序列扩增,但在其他几个基因中鉴定出27个罕见(次要等位基因频率<1%)的错义编码变异。一名患者在VCP基因中携带p.R95C错义突变,另一名患者在VCP基因中携带先前报道的p.I27V错义突变。VCP基因突变会导致与骨佩吉特病(PDB)和额颞叶痴呆(IBMPFD)相关的IBM。这两名患者均无肌无力家族史,也未表现出VCP基因突变所报道的其他症状,如PDB或痴呆。对这些VCP变异体的体外分析发现,它们与其他致病突变一样,均破坏了自噬。虽然sIBM发病机制中尚未明确涉及具体的遗传病因,但我们的研究表明,sIBM的基因评估在临床上可能具有重要意义,并有助于深入了解其发病机制。