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• W2101780101 abstract "A bstract : Therapy for mitochondrial diseases is woefully inadequate. How‐ever, lack of cure does not equate with lack of treatment. In this review, we consider sequentially several different therapeutic approaches. Palliative therapy is dictated by good medical practice and includes anticonvulsant medication, control of endocrine dysfunction, and surgical procedures. Removal of noxious metabolites is centered on combating lactic acidosis, but it extends to other metabolites, such as thymidine in patients with the mitochondrial neurogastrointestinal encephalomyopathy syndrome. Attempts to bypass blocks in the respiratory chain by administration of artificial electron acceptors have not been successful, but this concept may be amenable to genetic engineering. Administration of metabolites and cofactors is the mainstay of real‐life therapy and includes both components of the respiratory chain and other natural compounds. There is increasing interest in the administration of reactive oxygen species scavengers both in primary mitochondrial diseases and in neurodegenerative diseases directly or indirectly related to mitochondrial dysfunction. Aerobic exercise and physical therapy prevent or correct deconditioning and improve exercise tolerance in patients with mitochondrial myopathies due to mtDNA mutations. Gene therapy is a challenge because of polyplasmy and heteroplasmy, but interesting experimental approaches are being pursued and include, for example, decreasing the ratio of mutant to wild‐type mitochondrial genomes (gene shifting), converting mutated mtDNA genes into normal nDNA genes (allotropic expression), importing cognate genes from other species, or correcting mtDNA mutations with specific restriction endonucleases. Germline therapy raises ethical problems but is being seriously considered to prevent maternal transmission of mtDNA mutations. Preventive therapy through genetic counseling and prenatal diagnosis is still limited for mtDNA‐related disorders but is becoming increasingly important for nDNA‐related disorders." @default.
• W2101780101 created "2016-06-24" @default.
• W2101780101 creator A5026772758 @default.
• W2101780101 creator A5055048928 @default.
• W2101780101 creator A5070509047 @default.
• W2101780101 date "2004-04-01" @default.
• W2101780101 modified "2023-09-27" @default.
• W2101780101 title "Mitochondrial Encephalomyopathies: Therapeutic Approach" @default.
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• W2101780101 doi "https://doi.org/10.1196/annals.1293.023" @default.
• W2101780101 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15126300" @default.
• W2101780101 hasPublicationYear "2004" @default.
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