Logo image
Biallelic variants in COQ7 cause distal hereditary motor neuropathy with upper motor neuron signs
Journal article   Open access   Peer reviewed

Biallelic variants in COQ7 cause distal hereditary motor neuropathy with upper motor neuron signs

Adriana P. Rebelo, Pedro J. Tomaselli, Jessica Medina, Ying Wang, Maike F. Dohrn, Eva Nyvltova, Matt C. Danzi, Mark Garrett, Sean E. Smith, Alan Pestronk, …
Brain (London, England : 1878), Vol.146(10), pp.4191-4199
10/03/2023
DOI: 10.1093/brain/awad158
PMCID: PMC10545612
PMID: 37170631
url
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10545612View
Published (Version of record) Open Access

Abstract

Rebelo et al. identify COQ7 biallelic variants in nine families diagnosed with distal hereditary motor neuropathy with upper motor neuron involvement, thereby expanding the clinical phenotype associated with defects in this gene. COQ7 encodes a hydroxylase responsible for the penultimate step of coenzyme Q10 (CoQ(10)) biosynthesis in mitochondria. CoQ(10) is essential for multiple cellular functions, including mitochondrial oxidative phosphorylation, lipid metabolism, and reactive oxygen species homeostasis. Mutations in COQ7 have been previously associated with primary CoQ(10) deficiency, a clinically heterogeneous multisystemic mitochondrial disorder. We identified COQ7 biallelic variants in nine families diagnosed with distal hereditary motor neuropathy with upper neuron involvement, expending the clinical phenotype associated with defects in this gene. A recurrent p.Met1? change was identified in five families from Brazil with evidence of a founder effect. Fibroblasts isolated from patients revealed a substantial depletion of COQ7 protein levels, indicating protein instability leading to loss of enzyme function. High-performance liquid chromatography assay showed that fibroblasts from patients had reduced levels of CoQ(10), and abnormal accumulation of the biosynthetic precursor DMQ(10). Accordingly, fibroblasts from patients displayed significantly decreased oxygen consumption rates in patients, suggesting mitochondrial respiration deficiency. Induced pluripotent stem cell-derived motor neurons from patient fibroblasts showed significantly increased levels of extracellular neurofilament light protein, indicating axonal degeneration. Our findings indicate a molecular pathway involving CoQ(10) biosynthesis deficiency and mitochondrial dysfunction in patients with distal hereditary motor neuropathy. Further studies will be important to evaluate the potential benefits of CoQ(10) supplementation in the clinical outcome of the disease.
Clinical Neurology Life Sciences & Biomedicine Neurosciences Neurosciences & Neurology Science & Technology

Details

Metrics

Logo image