Bi-Allelic COQ4 Variants Cause Adult-Onset Ataxia-Spasticity Spectrum Disease.


Journal

Movement disorders : official journal of the Movement Disorder Society
ISSN: 1531-8257
Titre abrégé: Mov Disord
Pays: United States
ID NLM: 8610688

Informations de publication

Date de publication:
10 2022
Historique:
revised: 11 05 2022
received: 13 12 2021
accepted: 21 06 2022
pubmed: 2 9 2022
medline: 19 10 2022
entrez: 1 9 2022
Statut: ppublish

Résumé

COQ4 codes for a mitochondrial protein required for coenzyme Q In-house exome and genome datasets (n = 14,303) were screened for patients with bi-allelic variants in COQ4. Work-up included clinical characterization and functional studies in patient-derived cell lines. Six different COQ4 variants, three of them novel, were identified in six adult patients from four different families. Three patients had a phenotype of hereditary spastic paraparesis, two sisters showed a predominant cerebellar ataxia, and one patient had mild signs of both. Studies in patient-derived fibroblast lines revealed significantly reduced amounts of COQ4 protein, decreased CoQ We report bi-allelic variants in COQ4 causing an adult-onset ataxia-spasticity spectrum phenotype and a disease course much milder than previously reported. © 2022 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

Sections du résumé

BACKGROUND
COQ4 codes for a mitochondrial protein required for coenzyme Q
METHODS
In-house exome and genome datasets (n = 14,303) were screened for patients with bi-allelic variants in COQ4. Work-up included clinical characterization and functional studies in patient-derived cell lines.
RESULTS
Six different COQ4 variants, three of them novel, were identified in six adult patients from four different families. Three patients had a phenotype of hereditary spastic paraparesis, two sisters showed a predominant cerebellar ataxia, and one patient had mild signs of both. Studies in patient-derived fibroblast lines revealed significantly reduced amounts of COQ4 protein, decreased CoQ
CONCLUSION
We report bi-allelic variants in COQ4 causing an adult-onset ataxia-spasticity spectrum phenotype and a disease course much milder than previously reported. © 2022 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

Identifiants

pubmed: 36047608
doi: 10.1002/mds.29167
doi:

Substances chimiques

COQ4 protein, human 0
Mitochondrial Proteins 0
Ubiquinone 1339-63-5

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2147-2153

Informations de copyright

© 2022 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

Références

Doimo M, Desbats MA, Cerqua C, Cassina M, Trevisson E, Salviati L. Genetics of coenzyme q10 deficiency. Mol Syndromol 2014;5(3-4):156-162.
Alcázar-Fabra M, Trevisson E, Brea-Calvo G. Clinical syndromes associated with coenzyme Q10 deficiency. Essays Biochem 2018;62(3):377-398.
Banh RS, Kim ES, Spillier Q, et al. The polar oxy-metabolome reveals the 4-hydroxymandelate CoQ10 synthesis pathway. Nature 2021;597(7876):420-425.
Marbois B, Gin P, Gulmezian M, Clarke CF. The yeast Coq4 polypeptide organizes a mitochondrial protein complex essential for coenzyme Q biosynthesis. Biochimica et Biophysica Acta (BBA)-molecular and cell biology of. Lipids 2009;1791(1):69-75.
Brea-Calvo G, Haack TB, Karall D, et al. COQ4 mutations cause a broad spectrum of mitochondrial disorders associated with CoQ10 deficiency. Am J Hum Genet 2015;96(2):309-317.
Chung WK, Martin K, Jalas C, et al. Mutations in COQ4, an essential component of coenzyme Q biosynthesis, cause lethal neonatal mitochondrial encephalomyopathy. J Med Genet 2015;52(9):627-635.
Sondheimer N, Hewson S, Cameron JM, et al. Novel recessive mutations in COQ4 cause severe infantile cardiomyopathy and encephalopathy associated with CoQ10 deficiency. Mol Genet Metab Rep 2017;12:23-27.
Lu M, Zhou Y, Wang Z, Xia Z, Ren J, Guo Q. Clinical phenotype, in silico and biomedical analyses, and intervention for an east Asian population-specific c. 370G> a (p. G124S) COQ4 mutation in a Chinese family with CoQ10 deficiency-associated Leigh syndrome. J Hum Genet 2019;64(4):297-304.
Bosch AM, Kamsteeg E-J, Rodenburg RJ, et al. Coenzyme Q10 deficiency due to a COQ4 gene defect causes childhood-onset spinocerebellar ataxia and stroke-like episodes. Mol Genet Metab Rep 2018;17:19-21.
Caglayan AO, Gumus H, Sandford E, et al. COQ4 mutation leads to childhood-onset ataxia improved by CoQ10 administration. Cerebellum 2019;18(3):665-669.
Richards S, Aziz N, Bale S, et al. Standards and guidelines for the interpretation of sequence variants: a joint consensus recommendation of the American College of Medical Genetics and Genomics and the Association for Molecular Pathology. Genet Med 2015;17(5):405-423.
Hanisch F, Müller T, Muser A, Deschauer M, Zierz S. Lactate increase and oxygen desaturation in mitochondrial disorders-evaluation of two diagnostic screening protocols. J Neurol 2006;253(4):417-423.
Herebian D, Seibt A, Smits SH, et al. Detection of 6-demethoxyubiquinone in CoQ10 deficiency disorders: insights into enzyme interactions and identification of potential therapeutics. Mol Genet Metab 2017;121(3):216-223.
Mayr JA, Havlíčková V, Zimmermann F, et al. Mitochondrial ATP synthase deficiency due to a mutation in the ATP5E gene for the F1 ε subunit. Hum Mol Genet 2010;19(17):3430-3439.
Husain RA, Grimmel M, Wagner M, et al. Bi-allelic HPDL variants cause a neurodegenerative disease ranging from neonatal encephalopathy to adolescent-onset spastic paraplegia. Am J Hum Genet 2020;107(2):364-373.
Mero S, Salviati L, Leuzzi V, et al. New pathogenic variants in COQ4 cause ataxia and neurodevelopmental disorder without detectable CoQ 10 deficiency in muscle or skin fibroblasts. J Neurol 2021;268(9):3381-3389.
Hashemi SS, Zare-Abdollahi D, Bakhshandeh MK, et al. Clinical spectrum in multiple families with primary COQ10 deficiency. Am J Med Genet A 2021;185(2):440-452.
Laugwitz L, Seibt A, Herebian D, et al. Human COQ4 deficiency: delineating the clinical, metabolic and neuroimaging phenotypes. J Med Genet 2021. https://jmg.bmj.com/content/early/2021/12/20/jmedgenet-2021-107729.abstract.
Salviati L, Trevisson E, Doimo M, Navas P. Primary coenzyme Q10 deficiency. 2017.
Traschütz A, Schirinzi T, Laugwitz L, et al. Clinico-genetic, imaging and molecular delineation of COQ8A-ataxia: a multicenter study of 59 patients. Ann Neurol 2020;88(2):251-263.
Mantle D, Hargreaves IP. Ataxia and coenzyme Q10: an overview. Br J Neurosci Nurs 2018;14(3):108-114.
Galatolo D, Tessa A, Filla A, Santorelli FM. Clinical application of next generation sequencing in hereditary spinocerebellar ataxia: increasing the diagnostic yield and broadening the ataxia-spasticity spectrum. A retrospective analysis. Neurogenetics 2018;19(1):1-8.
Synofzik M, Schüle R. Overcoming the divide between ataxias and spastic paraplegias: shared phenotypes, genes, and pathways. Mov Disord 2017;32(3):332-345.
Marras C, Lang A, van de Warrenburg BP, et al. Nomenclature of genetic movement disorders: recommendations of the international Parkinson and movement disorder society task force. Mov Disord 2016;31(4):436-457.
Buján N, Arias A, Montero R, et al. Characterization of CoQ10 biosynthesis in fibroblasts of patients with primary and secondary CoQ10 deficiency. J Inherited Metab Dis 2014;37(1):53-62.
Horvath R, Czermin B, Gulati S, et al. Adult-onset cerebellar ataxia due to mutations in CABC1/ADCK3. J Neurol Neurosurg Psychiatry 2012;83(2):174-178.
Barca E, Musumeci O, Montagnese F, et al. Cerebellar ataxia and severe muscle CoQ10 deficiency in a patient with a novel mutation in ADCK3. Clin Genet 2016;90(2):156-160.
Wang Y, Smith C, Parboosingh JS, Khan A, Innes M, Hekimi S. Pathogenicity of two COQ7 mutations and responses to 2, 4-dihydroxybenzoate bypass treatment. J Cell Mol Med 2017;21(10):2329-2343.

Auteurs

Isabell Cordts (I)

Department of Neurology, Klinikum rechts der Isar, Technical University Munich, Munich, Germany.

Luisa Semmler (L)

Department of Neurology, Klinikum rechts der Isar, Technical University Munich, Munich, Germany.

Jannik Prasuhn (J)

Department of Neurology, Center for Brain, Behavior, and Metabolism, University Medical Center Schleswig-Holstein, Lübeck, Germany.
Institute of Neurogenetics, University Medical Center Schleswig-Holstein, Lübeck, Germany.

Annette Seibt (A)

Department of General Pediatrics, Neonatology, and Pediatric Cardiology, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany.

Diran Herebian (D)

Department of General Pediatrics, Neonatology, and Pediatric Cardiology, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany.

Tharsini Navaratnarajah (T)

Department of General Pediatrics, Neonatology, and Pediatric Cardiology, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany.

Joohyun Park (J)

Institute of Medical Genetics and Applied Genomics, University of Tübingen, Tübingen, Germany.

Natalie Deininger (N)

Institute of Medical Genetics and Applied Genomics, University of Tübingen, Tübingen, Germany.

Lucia Laugwitz (L)

Institute of Medical Genetics and Applied Genomics, University of Tübingen, Tübingen, Germany.
Department of Neuropediatrics, Developmental Neurology, and Social Pediatrics, University of Tübingen, Tübingen, Germany.

Sophia L Göricke (SL)

Institute of Diagnostic and Interventional Radiology and Neuroradiology, Essen University Hospital, University of Duisburg-Essen, Essen, Germany.

Paul Lingor (P)

Department of Neurology, Klinikum rechts der Isar, Technical University Munich, Munich, Germany.

Norbert Brüggemann (N)

Department of Neurology, Center for Brain, Behavior, and Metabolism, University Medical Center Schleswig-Holstein, Lübeck, Germany.
Institute of Neurogenetics, University Medical Center Schleswig-Holstein, Lübeck, Germany.

Alexander Münchau (A)

Institute of Systems Motor Science, University of Lübeck, Lübeck, Germany.

Matthis Synofzik (M)

Department of Neurodegeneration, Hertie Institute for Clinical Brain Research (HIH), University of Tübingen, Tübingen, Germany.
German Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany.

Dagmar Timmann (D)

Department of Neurology and Center for Translational Neuro- and Behavioral Sciences (C-TNBS), Essen University Hospital, Essen, Germany.

Johannes A Mayr (JA)

University Children's Hospital, Salzburger Landeskliniken and Paracelsus Medical University Salzburg, Salzburg, Austria.

Tobias B Haack (TB)

Institute of Medical Genetics and Applied Genomics, University of Tübingen, Tübingen, Germany.
Centre for Rare Diseases, University of Tübingen, Tübingen, Germany.

Felix Distelmaier (F)

Department of General Pediatrics, Neonatology, and Pediatric Cardiology, Medical Faculty, Heinrich-Heine-University, Düsseldorf, Germany.

Marcus Deschauer (M)

Department of Neurology, Klinikum rechts der Isar, Technical University Munich, Munich, Germany.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH