ArticleBrain : a journal of neurology2023
Homozygous COQ7 mutation: a new cause of potentially treatable distal hereditary motor neuropathy.
Article in Brain : a journal of neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 25 citations in OpenAlex.
- Immunological drivers of oxidative stress in glaucoma: implications for antioxidant therapy.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2026Review
- The weight of genotype on the clinical presentation of COQ7-related hereditary motor axonal neuropathy: a case series and literature review.Arquivos de neuro-psiquiatria · 2026Review
- Mitochondrial Dysfunctions in Human Primary Coenzyme QBiomolecules · 2026Review
- Homozygous COQ9 mutation: a new cause of potentially treatable hereditary spastic paraplegia.European journal of human genetics : EJHG · 2025Article
- Mutations of the Electron Transport Chain Affect Lifespan and ROS Levels inAntioxidants (Basel, Switzerland) · 2025Review
- Understanding coenzyme Q.Physiological reviews · 2024Review
- COQ7 defect causes prenatal onset of mitochondrial CoQEuropean journal of human genetics : EJHG · 2024Article
- Primary CoQ10 deficiency: treatable heterogeneous group of disorders.European journal of human genetics : EJHG · 2024Article
- A previously unreported NARS1 variant causes dominant distal hereditary motor neuropathy in a French family.Journal of the peripheral nervous system : JPNS · 2024Article
- Clinical, biochemical and molecular characterization of a new case withJIMD reports · 2024Article
- Case Report: Charcot-marie-tooth disease caused by aFrontiers in genetics · 2024Article
- COQ7 splice site variant causing a spastic paraparesis phenotype in siblings.Journal of genetics · 2024Article
- Phenotypic, molecular, and functional characterization of COQ7-related primary CoQMolecular genetics and metabolism · 2023Article
- A founder mutation in COQ7, p.(Leu111Pro), causes pure hereditary spastic paraplegia (HSP) in the Iranian population.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023Article
- Neuroimaging in Primary Coenzyme-QAntioxidants (Basel, Switzerland) · 2023Review
- Early onset hereditary neuronopathies: an update on non-5q motor neuron diseases.Brain : a journal of neurology · 2023Review
- Report on the 6th Ottawa International Conference on Neuromuscular Disease & Biology - September 7-9, 2023, Ottawa, Canada.Journal of neuromuscular diseasesArticle
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20 authors at 6 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Distal hereditary motor neuropathy represents a group of motor inherited neuropathies leading to distal weakness. We report a family of two brothers and a sister affected by distal hereditary motor neuropathy in whom a homozygous variant c.3G>T (p.1Met?) was identified in the COQ7 gene. This gene encodes a protein required for coenzyme Q10 biosynthesis, a component of the respiratory chain in mitochondria. Mutations of COQ7 were previously associated with severe multi-organ disorders characterized by early childhood onset and developmental delay. Using patient blood samples and fibroblasts derived from a skin biopsy, we investigated the pathogenicity of the variant of unknown significance c.3G>T (p.1Met?) in the COQ7 gene and the effect of coenzyme Q10 supplementation in vitro. We showed that this variation leads to a severe decrease in COQ7 protein levels in the patient's fibroblasts, resulting in a decrease in coenzyme Q10 production and in the accumulation of 6-demethoxycoenzyme Q10, the COQ7 substrate. Interestingly, such accumulation was also found in the patient's plasma. Normal coenzyme Q10 and 6-demethoxycoenzyme Q10 levels were restored in vitro by using the coenzyme Q10 precursor 2,4-dihydroxybenzoic acid, thus bypassing the COQ7 requirement. Coenzyme Q10 biosynthesis deficiency is known to impair the mitochondrial respiratory chain. Seahorse experiments showed that the patient's cells mainly rely on glycolysis to maintain sufficient ATP production. Consistently, the replacement of glucose by galactose in the culture medium of these cells reduced their proliferation rate. Interestingly, normal proliferation was restored by coenzyme Q10 supplementation of the culture medium, suggesting a therapeutic avenue for these patients. Altogether, we have identified the first example of recessive distal hereditary motor neuropathy caused by a homozygous variation in the COQ7 gene, which should thus be included in the gene panels used to diagnose peripheral inherited neuropathies. Furthermore, 6-demethoxycoenzyme Q10 accumulation in the blood can be used to confirm the pathogenic nature of the mutation. Finally, supplementation with coenzyme Q10 or derivatives should be considered to prevent the progression of COQ7-related peripheral inherited neuropathy in diagnosed patients.
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