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Research Article

CHCHD10 is not a frequent causative gene in Chinese ALS patients

, , , , , , , , & show all
Pages 458-460 | Received 28 Jan 2016, Accepted 24 Feb 2016, Published online: 14 Apr 2016

References

  • Siddique T, Deng HX. Genetics of amyotrophic lateral sclerosis. Hum Mol Genet. 1996;5:1465–70.
  • Wong CH, Topp S, Gkazi AS, Troakes C, Miller JW, de Majo M, et al. The CHCHD10 P34S variant is not associated with ALS in a UK cohort of familial and sporadic patients. Neurobiol Aging. 2015;36:2908.
  • Bannwarth S, Ait-El-Mkadem S, Chaussenot A, Genin EC, LacasGervais S, Fragaki K, et al. A mitochondrial origin for frontotemporal dementia and amyotrophic lateral sclerosis through CHCHD10 involvement. Brain. 2014;137:2329–45.
  • Müller K, Andersen PM, Hülbers A, Marroquin N, Volk AE, Danzer KM, et al. Two novel mutations in conserved codons indicate that CHCHD10 is a gene associated with motor neuron disease. Brain. 2014;137:1–3.
  • Chaussenot A, Le Ber I, Ait-El-Mkadem S, Camuzat A, de Septenville A, Bannwarth S, et al. Screening of CHCHD10 in a French cohort confirms the involvement of this gene in frontotemporal dementia with amyotrophic lateral sclerosis patients. Neurobiol Aging. 2014;35:2884.e1-4.
  • Johnson JO, Glynn SM, Gibbs JR, Nalls MA, Sabatelli M, Restagno G, et al. Mutations in the CHCHD10 gene are a common cause of familial amyotrophic lateral sclerosis. Brain. 2014;137:1–2.
  • Ronchi D, Riboldi G, del Bo R, Ticozzi N, Scarlato M, Galimberti D, et al. CHCHD10 mutations in Italian patients with sporadic amyotrophic lateral sclerosis. Brain. 2015;138:1–4.
  • Dols-Icardo O, Nebot I, Gorostidi A, Ortega-Cubero S, Hernández I, Rojas-Garcıá R, et al. Analysis of the CHCHD10 gene in patients with frontotemporal dementia and amyotrophic lateral sclerosis from Spain. Brain. 2015; 138:e400.
  • Brooks BR, Miller RG, Swash M, Munsat TL. El Escorial revisited: revised criteria for the diagnosis of amyotrophic lateral sclerosis. Amyotroph Lateral Scler Other Motor Neuron Disord. 2000;1:293–9.
  • Majoor-Krakauer D, Willems PJ, Hofman A. Genetic epidemiology of amyotrophic lateral sclerosis. Clin Genet. 2003;63:83–101.
  • Andersen PM, Al-Chalabi A. Clinical genetics of amyotrophic lateral sclerosis: what do we really know? Nat Rev Neurol. 2011;7:603–15.
  • Ajroud-Driss S, Fecto F, Ajroud K, Lalani I, Calvo SE, Mootha VK, et al. Mutation in the novel nuclear-encoded mitochondrial protein CHCHD10 in a family with autosomal dominant mitochondrial myopathy. Neurogenetics. 2015;16:1–9.
  • Pizzuti A, Petrucci S. Mitochondrial dysfunction as a cause of ALS. Arch Ital Biol. 2011;149:113–19.
  • Shi P, Wei Y, Zhang J, Gal J, Zhu H. Mitochondrial Dysfunction is a Converging Point of Multiple Pathological Pathways in Amyotrophic Lateral Sclerosis. Journal of Alzheimer’s Disease. 2010;20:S311–S24.
  • Cozzolino M, Ferri A, Valle C, Carrì MT. Mitochondrial dysfunction is a converging point of multiple pathological pathways in amyotrophic lateral sclerosis. J Alzheimers Dis. 2010; (Suppl 2):S311–24.
  • Cozzolino M, Ferri A, Valle C, Carrì MT. Mitochondria and ALS: implications from novel genes and pathways. Mol Cell Neurosci. 2013;55:44–9.
  • Pasanen P, Myllykangas L, Pöyhönen M, Kiuru-Enari S, Tienari PJ, Laaksovirta H, et al. Intrafamilial clinical variability in individuals carrying the CHCHD10 mutation Gly66Val. Acta Neurol Scand. 2016;133(5):361–6.

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