Maike F Dohrn, Corina Heller, Diana Zengeler, Carolin D Obermaier, Saskia Biskup, Joachim Weis, Stefan Nikolin, Kristl G Claeys, Ulrike Schöne, Danique Beijer, Natalie Winter, Pascal Achenbach, Burkhard Gess, Jörg B Schulz, Lejla Mulahasanovic
{"title":"杂合POLG变异Ser1181Asn在常染色体显性轴突神经病、近端肌肉疲劳、上睑下垂和红色纤维粗糙的家族中共分离。","authors":"Maike F Dohrn, Corina Heller, Diana Zengeler, Carolin D Obermaier, Saskia Biskup, Joachim Weis, Stefan Nikolin, Kristl G Claeys, Ulrike Schöne, Danique Beijer, Natalie Winter, Pascal Achenbach, Burkhard Gess, Jörg B Schulz, Lejla Mulahasanovic","doi":"10.1186/s42466-022-00169-w","DOIUrl":null,"url":null,"abstract":"<p><p>By whole-exome sequencing, we found the heterozygous POLG variant c.3542G>A; p.Ser1181Asn in a family of four affected individuals, presenting with a mixed neuro-myopathic phenotype. The variant is located within the active site of polymerase gamma, in a cluster region associated with an autosomal dominant inheritance. In adolescence, the index developed distal atrophies and weakness, sensory loss, afferent ataxia, double vision, and bilateral ptosis. One older sister presented with Charcot-Marie-Tooth-like symptoms, while the youngest sister and father reported exercise-induced muscle pain and proximal weakness. In none of the individuals, we observed any involvement of the central nervous system. Muscle biopsies obtained from the father and the older sister showed ragged-red fibers, and electron microscopy confirmed mitochondrial damage. We conclude that this novel POLG variant explains this family's phenotype.</p>","PeriodicalId":19169,"journal":{"name":"Neurological Research and Practice","volume":" ","pages":"5"},"PeriodicalIF":0.0000,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8805222/pdf/","citationCount":"3","resultStr":"{\"title\":\"Heterozygous POLG variant Ser1181Asn co-segregating in a family with autosomal dominant axonal neuropathy, proximal muscle fatigability, ptosis, and ragged red fibers.\",\"authors\":\"Maike F Dohrn, Corina Heller, Diana Zengeler, Carolin D Obermaier, Saskia Biskup, Joachim Weis, Stefan Nikolin, Kristl G Claeys, Ulrike Schöne, Danique Beijer, Natalie Winter, Pascal Achenbach, Burkhard Gess, Jörg B Schulz, Lejla Mulahasanovic\",\"doi\":\"10.1186/s42466-022-00169-w\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>By whole-exome sequencing, we found the heterozygous POLG variant c.3542G>A; p.Ser1181Asn in a family of four affected individuals, presenting with a mixed neuro-myopathic phenotype. The variant is located within the active site of polymerase gamma, in a cluster region associated with an autosomal dominant inheritance. In adolescence, the index developed distal atrophies and weakness, sensory loss, afferent ataxia, double vision, and bilateral ptosis. One older sister presented with Charcot-Marie-Tooth-like symptoms, while the youngest sister and father reported exercise-induced muscle pain and proximal weakness. In none of the individuals, we observed any involvement of the central nervous system. Muscle biopsies obtained from the father and the older sister showed ragged-red fibers, and electron microscopy confirmed mitochondrial damage. We conclude that this novel POLG variant explains this family's phenotype.</p>\",\"PeriodicalId\":19169,\"journal\":{\"name\":\"Neurological Research and Practice\",\"volume\":\" \",\"pages\":\"5\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2022-02-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8805222/pdf/\",\"citationCount\":\"3\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neurological Research and Practice\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1186/s42466-022-00169-w\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neurological Research and Practice","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1186/s42466-022-00169-w","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Heterozygous POLG variant Ser1181Asn co-segregating in a family with autosomal dominant axonal neuropathy, proximal muscle fatigability, ptosis, and ragged red fibers.
By whole-exome sequencing, we found the heterozygous POLG variant c.3542G>A; p.Ser1181Asn in a family of four affected individuals, presenting with a mixed neuro-myopathic phenotype. The variant is located within the active site of polymerase gamma, in a cluster region associated with an autosomal dominant inheritance. In adolescence, the index developed distal atrophies and weakness, sensory loss, afferent ataxia, double vision, and bilateral ptosis. One older sister presented with Charcot-Marie-Tooth-like symptoms, while the youngest sister and father reported exercise-induced muscle pain and proximal weakness. In none of the individuals, we observed any involvement of the central nervous system. Muscle biopsies obtained from the father and the older sister showed ragged-red fibers, and electron microscopy confirmed mitochondrial damage. We conclude that this novel POLG variant explains this family's phenotype.