Mitochondria in neuroinflammation – Multiple sclerosis (MS), leber hereditary optic neuropathy (LHON) and LHON-MS. (25th September 2019)

• Record Type: Journal Article
• Authors: Bargiela, David; Chinnery, Patrick F
• Is Part Of: Neuroscience letters. Volume 710(2019)
• Publication Date: 2019-09-25
• Subjects: ATP adenosine triphosphate -- LHON Leber's Hereditary Optic Neuropathy -- MS multiple sclerosis -- mtDNA mitochondrial DNA -- SNP single nucleotide polymorphism; Mitochondria -- Multiple sclerosis -- Leber's hereditary optic neuropathy -- LHON-MS -- Harding's disease -- Neuroinflammation -- Neurodegeneration; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2017.06.051
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: Mitochondrial damage can be both inherited and acquired. The role of mitochondria as drivers of neuroinflammation remains unresolved. There is overlap in the clinical and molecular mechanisms of MS and LHON. Mitochondrial pathways may represent potential therapeutic targets in MS. Abstract: Mitochondrial dysfunction is associated with neuroinflammation and neurodegenerative disease, but its role as a driver in these processes is uncertain. Understanding the pathogenesis of inherited mitochondrial disorders may help us to uncover mechanisms involved during acquired mitochondrial dysfunction. We review the mechanisms of mitochondrial dysfunction in Leber's hereditary optic neuropathy and multiple sclerosis and discuss shared clinical and molecular features in both conditions. Targeting mitochondrial pathways involved in inflammation or apoptosis may be a possible therapeutic approach in multiple sclerosis.