Abstract
Charcot-Marie-Tooth disease is a genetically heterogeneous group of motor and sensory neuropathies associated with mutations in more than 30 genes. Charcot-Marie-Tooth disease type 4J (OMIM 611228) is a recessive, potentially severe form of the disease caused by mutations of the lipid phosphatase FIG4. We provide a more complete view of the features of this disorder by describing 11 previously unreported patients with Charcot-Marie-Tooth disease type 4J. Three patients were identified from a small cohort selected for screening because of their early onset disease and progressive proximal as well as distal weakness. Eight patients were identified by large-scale exon sequencing of an unselected group of 4000 patients with Charcot-Marie-Tooth disease. In addition, 34 new FIG4 variants were detected. Ten of the new CMT4J cases have the compound heterozygous genotype FIG4(I41T/null) described in the original four families, while one has the novel genotype FIG4(L17P/nul)(l). The population frequency of the I41T allele was found to be 0.001 by genotyping 5769 Northern European controls. Thirty four new variants of FIG4 were identified. The severity of Charcot-Marie-Tooth disease type 4J ranges from mild clinical signs to severe disability requiring the use of a wheelchair. Both mild and severe forms have been seen in patients with the same genotype. The results demonstrate that Charcot-Marie-Tooth disease type 4J is characterized by highly variable onset and severity, proximal as well as distal and asymmetric muscle weakness, electromyography demonstrating denervation in proximal and distal muscles, and frequent progression to severe amyotrophy. FIG4 mutations should be considered in Charcot-Marie-Tooth patients with these characteristics, especially if found in combination with sporadic or recessive inheritance, childhood onset and a phase of rapid progression.
MeSH Terms
Adult
Australia
Charcot-Marie-Tooth Disease/classification,complications,diagnosis,genetics
Child
Child, Preschool
Exons/genetics
Family Health
Female
Flavoproteins/genetics
Foot Deformities/etiology,genetics
Genotype
Glutamic Acid/genetics
Humans
Lysine/genetics
Male
Middle Aged
Models, Molecular
Muscle Weakness/etiology,genetics
Mutation/genetics
Neural Conduction/genetics
Phenotype
Phosphoric Monoester Hydrolases
Sural Nerve/pathology,ultrastructure
Chemicals
Flavoproteins
Glutamic Acid
FIG4 protein, human
Phosphoric Monoester Hydrolases
Lysine
Authors & Affiliations
16 authors, click to expand affiliations / ORCID
Nicholson Garth
Department of Neurology, University of Sydney, ANZAC Institute, Concord Hospital, NSW 2139, Australia.
Lenk Guy M
Reddel Stephen W
Grant Adrienne E
Towne Charles F
Ferguson Cole J
Simpson Ericka
Scheuerle Angela
Yasick Michelle
Hoffman Stuart
Blouin Randall
Brandt Carla
Coppola Giovanni
Biesecker Leslie G
Batish Sat D
Meisler Miriam H
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