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Disease Info Card
Leigh Disease
Information about Leigh Disease: characteristics, related genes and pathways, plus antibodies you can use for research. This page is being enriched constantly, if you see some information you would like this page to include please send your suggestions to us.
Overview of Leigh Disease
Most recent studies have shown that Leigh Disease shares some biological mechanisms with acidosis, acidosis-lactic, ataxia, atrophy, brain-diseases, brain-diseases-metabolic, cytochrome-c-oxidase-deficiency, encephalomalacia, encephalopathies, epilepsy, melas-syndrome, mitochondrial-diseases, mitochondrial-encephalomyopathies, muscle-hypotonia, myopathy, neurodegenerative-disorders, nicotinamide-adenine-dinucleotide-coenzyme-q-reductase-deficiency.
Among the many pathways, these few ones have gauged particular interests from scientists studying Leigh Disease, and have been seen in publications frequently: Aging, Brain Development, Cardiac Conduction, Electron Transport, Electron Transport Chain, Excretion, Fatty Acid Oxidation, Gluconeogenesis, Glycolysis, Localization, Mitochondrial Translation, Muscle Atrophy, Myelination, Oogenesis, Oxidative Phosphorylation, Pathogenesis, Pyruvate Oxidation, Regeneration, Translation, Transport
Quite a number of genes have been found to play important roles in Leigh Disease, such as COX5A, COX8A, CPOX, CSF2, CYCS, DLD, LAMC2, LIAS, LRPPRC, MT-ATP6, NDUFS4, NDUFS7, NPTX2, PC, PDP1, POLG, SCO2, SURF1. See what Boster has to offer for the research of these genes by clicking the gene name links below and view a more detailed info card/product listing for that gene.
In a later update, we will include information such as current drugs and therapy solutions as well as on-going and past clinical trials for this disease. Plesae stay updated.