Mitochondrial function and epigenetic outlook in Leber's Hereditary Optic Neuropathy (LHON)

Abstract Introduction Neurodegenerative diseases are reliant on neurons which demand high energy for its functioning, which depends on systems like mitochondrial oxidative phosphorylation (OXPHOS). This energy generated by mitochondria occurs through different respiratory complexes ranging from complex I to IV. Complexes are also known as NADH, including complex I because it is the first enzyme and largest chain of the given respiratory chain; however, complex 1 is called the ubiquinone oxidoreductase. Majority of neurodegenerative cases demonstrate irresistible evidence of plenty of mitochondrial subtleties that are impaired, as inhibition of complex 1 could lead to excessive reactive oxygen species (ROS) production. Development In this review we try to discuss on how epigenetic modifications could cause a drift in smooth functioning of mitochondria and its function leading to neurodegenerative diseases like Leber's hereditary optic neuropathy (LHON). The reference articles were collected from NCBI-Pubmed, Scopus and Web of science. This review tries to deliver a summarizing overview related to Complex 1 mediated mitochondrial dysfunction and studies done so far in this aspect, along with the epigenetic modifications. Conclusion In this review we discussed the different roles of mitochondria and its related dysfunction in the pathogenesis of neurodegenerative diseases.