Abstract
Metabolic optic neuropathies present in a very similar fashion but yet show some distinct variations. Investigations have revealed that the common pathologic basis of these optic neuropathies is a dysfunction of oxidative phosphorylation in mitochondria leading to retinal ganglion cell degeneration. This impairment can be genetic or acquired. Leber’s hereditary optic neuropathy and dominant optic atrophy are the two primary inherited optic neuropathies, whereas acquired metabolic optic neuropathies can be due to toxins or nutritional deficiencies. Mitochondria are remarkable cytoplasmic organelles carrying their own DNA and are also influenced by nuclear DNA. The genetic background is pivotal in understanding the molecular mechanisms and the wide spectrum of clinical phenotypes of these disorders. Understanding the genetic, environmental and epigenetic interplays will be important for the development of therapeutic strategies aimed to protect against retinal ganglion cell death.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
