Dysmyelinating and demyelinating Charcot–Marie–Tooth disease associated with two myelin protein zero gene mutations

Journal of Applied Genetics - Tập 52 - Trang 177-183 - 2010
Hanna Drac1,2, Dagmara Kabzińska1, Izabela Moszyńska1, Halina Strugalska-Cynowska1, Irena Hausmanowa-Petrusewicz1, Andrzej Kochański1
1Neuromuscular Unit, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland
2Department of Neurology, Medical University of Warsaw, Warsaw, Poland

Tóm tắt

Mutations in the myelin protein zero (MPZ) gene are the third most frequent cause of hereditary motor and sensory neuropathies (HMSN), also called Charcot–Marie–Tooth disorders (CMT). Only in case of recurrent mutations occurring in the MPZ gene is it possible to draw phenotype–genotype correlations essential for establishing the prognosis and outcomes of CMT1. We have surveyed a cohort of 67 Polish patients from CMT families with demyelinating neuropathy for mutations in the MPZ gene. In this study, we report two CMT families in which the Ile135Thr and Pro132Leu mutations have been identified for the MPZ gene. These MPZ gene mutations had not been identified hitherto in the Polish population. The Pro132Leu mutation segregates with a severe early-onset dysmyelinating–hypomyelinating neuropathy, whereas the Ile135Thr substitution is associated with the classical phenotype of CMT1. To the best of our knowledge, we present here, for the first time, morphological data obtained in two sural nerve biopsies pointing to a hypomyelination–dysmyelination process in a family harboring the Pro132Leu mutation in the MPZ gene.

Tài liệu tham khảo

Aarskog NK, Vedeler CA (2000) Real-time quantitative polymerase chain reaction. A new method that detects both the peripheral myelin protein 22 duplication in Charcot–Marie–Tooth type 1A disease and the peripheral myelin protein 22 deletion in hereditary neuropathy with liability to pressure palsies. Hum Genet 107(5):494–498 Barisic N, Claeys KG, Sirotković-Skerlev M et al (2008) Charcot–Marie–Tooth disease: a clinico-genetic confrontation. Ann Hum Genet 72(Pt 3):416–441 Filbin MT, Walsh FS, Trapp BD et al (1990) Role of myelin P0 protein as a homophilic adhesion molecule. Nature 344(6269):871–872 Greenberg SA, Walsh RJ (2005) Molecular diagnosis of inheritable neuromuscular disorders. Part II: application of genetic testing in neuromuscular disease. Muscle Nerve 31:431–451 Harding AE, Thomas PK (1980) The clinical features of hereditary motor and sensory neuropathy types I and II. Brain 103(2):259–280 Inherited Peripheral Neuropathies Mutation Database (IPNMDB) (2007) Home page at: http://www.molgen.ua.ac.be/cmtmutations/ Mersiyanova IV, Ismailov SM, Polyakov AV et al (2000) Screening for mutations in the peripheral myelin genes PMP22, MPZ and Cx32 (GJB1) in Russian Charcot–Marie–Tooth neuropathy patients. Hum Mutat 15:340–347 Miller SA, Dykes DD, Polesky HF (1988) A simple salting out procedure for extracting DNA from human nucleated cells. Nuc Acid Res 16(3):1215 Moszyńska I, Kabzińska D, Sinkiewicz-Darol E et al (2009) A newly identified Thr99fsX110 mutation in the PMP22 gene associated with an atypical phenotype of the hereditary neuropathy with liability to pressure palsies. Acta Biochim Pol 56(4):627–630 Nelis E, Van Broeckhoven C, De Jonghe P et al (1996) Estimation of the mutation frequencies in Charcot–Marie–Tooth disease type 1 and hereditary neuropathy with liability to pressure palsies: a European collaborative study. Eur J Hum Genet 4(1):25–33 Roa BB, Warner LE, Garcia CA et al (1996) Myelin protein zero (MPZ) gene mutations in nonduplication type 1 Charcot–Marie–Tooth disease. Hum Mutat 7:36–45 Shy ME (2006) Peripheral neuropathies caused by mutations in the myelin protein zero. J Neurol Sci 242:55–66 Shy ME, Jáni A, Krajewski K et al (2004) Phenotypic clustering in MPZ mutations. Brain 127:371–384 Sorour E, Upadhyaya M (1998) Mutation analysis in Charcot–Marie–Tooth disease type 1 (CMT1). Hum Mutat 1:S242–S247 Tyson J, Ellis D, Fairbrother U et al (1997) Hereditary demyelinating neuropathy of infancy. A genetically complex syndrome. Brain 120:47–63