Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8962078 | Mitochondrion | 2018 | 29 Pages |
Abstract
MON needs to be appreciated, requires extensive diagnostic work-up, and supportive treatment should be applied although loss of vision, as the most severe outcome, can often not be prevented.
Keywords
LHONOPNVEPPCHCMTMIDWESRCCCharcot-Marie-Tooth diseaseIPSCsMELASRGCMDSKSSRNFLEMEAERGNBIACPEOCoQMERRFNARPADOAaroAMitochondrial depletion syndromeAIONROSautosomal dominant optic atrophyadenosin triphosphateATPmitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodesEuropean Medicine AgencyMitochondrial disorderelectroretinogramMRIOctneurodegeneration with brain iron accumulationTemMagnetic resonance imagingWhole exome sequencingOptical coherence tomographyCNSmtDNARespiratory chainSANDOInduced pluripotent stem cellsRetinal ganglion cellsKearns-Sayre SyndromeLeigh syndromeWolfram syndromecentral nervous systemOptic nerveOxidative phosphorylationRetinal nerve fiber layercerebro-spinal fluidCSFRespiratory chain complexMONMitochondrialTransmission electron microscopyLeber hereditary optic neuropathyAnterior ischemic optic neuropathyoptic neuropathyPosterior Ischemic Optic Neuropathyolivary pretectal nucleusPionChronic progressive external ophthalmoplegiaReactive oxygen species
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Authors
Josef Finsterer, Michelangelo Mancuso, Davide Pareyson, Jean-Marc Burgunder, Thomas Klopstock,