Reactive Oxygen Species in Mitochondrial Optic Neuropathies: Response.
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[1] N. Miller. Developing a Human Clinical Trial From a Scientific Hypothesis , 2015, Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society.
[2] L. Levin. Superoxide Generation Explains Common Features of Optic Neuropathies Associated With Cecocentral Scotomas , 2015, Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society.
[3] C. La Morgia,et al. Mitochondrial optic neuropathies: additional facts and concepts – response , 2014, Clinical & experimental ophthalmology.
[4] C. La Morgia,et al. Mitochondrial optic neuropathies: our travels from bench to bedside and back again , 2013, Clinical & experimental ophthalmology.
[5] V. Carelli,et al. Mathematically modeling the involvement of axons in Leber's hereditary optic neuropathy. , 2012, Investigative ophthalmology & visual science.
[6] M. Sharpley,et al. Mouse mtDNA mutant model of Leber hereditary optic neuropathy , 2012, Proceedings of the National Academy of Sciences.
[7] E. Wang,et al. Modelling the effects of age-related mtDNA mutation accumulation; complex I deficiency, superoxide and cell death. , 1995, Biochimica et biophysica acta.
[8] L. Levin. Mechanisms of retinal ganglion specific-cell death in Leber hereditary optic neuropathy. , 2007, Transactions of the American Ophthalmological Society.
[9] P. Win,et al. Leber's hereditary optic neuropathy differentially affects smaller axons in the optic nerve. , 2000, Transactions of the American Ophthalmological Society.