{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T12:54:32Z","timestamp":1787921672278,"version":"build-2784847793"},"reference-count":56,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2024,2,14]],"date-time":"2024-02-14T00:00:00Z","timestamp":1707868800000},"content-version":"vor","delay-in-days":44,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,3,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Mitochondrial myopathies are frequently recognized in childhood as part of a broader multisystem disorder and often overlooked in adulthood. Herein, we describe the phenotypic and genotypic spectrum and long-term outcomes of mitochondrial myopathies diagnosed in adulthood, focusing on neuromuscular features, electrodiagnostic and myopathological findings and survival. We performed a retrospective chart review of adult patients diagnosed with mitochondrial myopathy at Mayo Clinic (2005\u201321). We identified 94 patients. Median time from symptom onset to diagnosis was 11 years (interquartile range 4\u201321 years). Median age at diagnosis was 48 years (32\u201363 years). Primary genetic defects were identified in mitochondrial DNA in 48 patients (10 with single large deletion, 38 with point mutations) and nuclear DNA in 29. Five patients had multiple mitochondrial DNA deletions or depletion without nuclear DNA variants. Twelve patients had histopathological features of mitochondrial myopathy without molecular diagnosis. The most common phenotypes included multisystem disorder (n = 30); mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (14); limb myopathy (13); chronic progressive external ophthalmoplegia (12); and chronic progressive external ophthalmoplegia-plus (12). Isolated skeletal muscle manifestations occurred in 27%. Sixty-nine per cent had CNS and 21% had cardiac involvement. Mutations most frequently involved MT-TL1 (27) and POLG (17); however, a wide spectrum of established and novel molecular defects, with overlapping phenotypes, was identified. Electrodiagnostic studies identified myopathy (77%), fibrillation potentials (27%) and axonal peripheral neuropathy (42%, most common with nuclear DNA variants). Among 42 muscle biopsies available, median percentage counts were highest for cytochrome C oxidase negative fibres (5.1%) then ragged blue (1.4%) and ragged red fibres (0.5%). Skeletal muscle weakness was mild and slowly progressive (decline in strength summated score of 0.01\/year). Median time to gait assistance was 5.5 years from diagnosis and 17 years from symptom onset. Thirty patients died, with median survival of 33.4 years from symptom onset and 10.9 years from diagnosis. Median age at death was 55 years. Cardiac involvement was associated with increased mortality [hazard ratio 2.36 (1.05, 5.29)]. There was no difference in survival based on genotype or phenotype. Despite the wide phenotypic and genotypic spectrum, mitochondrial myopathies in adults share similar features with slowly progressive limb weakness, contrasting with common multiorgan involvement and high mortality.<\/jats:p>","DOI":"10.1093\/braincomms\/fcae041","type":"journal-article","created":{"date-parts":[[2024,2,12]],"date-time":"2024-02-12T16:28:40Z","timestamp":1707755320000},"source":"Crossref","is-referenced-by-count":14,"title":["Mitochondrial myopathies diagnosed in adulthood: clinico-genetic spectrum and long-term outcomes"],"prefix":"10.1093","volume":"6","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3512-1796","authenticated-orcid":false,"given":"Grayson","family":"Beecher","sequence":"first","affiliation":[{"name":"Department of Neurology, Mayo Clinic , Rochester, MN 55905 , USA"},{"name":"Division of Neurology, Department of Medicine, University of Alberta , Edmonton, Alberta , Canada T6G 2G3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ralitza H","family":"Gavrilova","sequence":"additional","affiliation":[{"name":"Department of Neurology, Mayo Clinic , Rochester, MN 55905 , USA"},{"name":"Department of Clinical Genomics, Mayo Clinic , Rochester, MN 55905 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jay","family":"Mandrekar","sequence":"additional","affiliation":[{"name":"Department of Neurology, Mayo Clinic , Rochester, MN 55905 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6212-1236","authenticated-orcid":false,"given":"Elie","family":"Naddaf","sequence":"additional","affiliation":[{"name":"Department of Neurology, Mayo Clinic , Rochester, MN 55905 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2024,2,14]]},"reference":[{"issue":"6158","key":"2024043010124865500_fcae041-B1","doi-asserted-by":"crossref","first-page":"717","DOI":"10.1038\/331717a0","article-title":"Deletions of muscle mitochondrial DNA in patients with mitochondrial myopathies","volume":"331","author":"Holt","year":"1988","journal-title":"Nature"},{"issue":"4884","key":"2024043010124865500_fcae041-B2","doi-asserted-by":"crossref","first-page":"1427","DOI":"10.1126\/science.3201231","article-title":"Mitochondrial DNA mutation associated with Leber\u2019s hereditary optic neuropathy","volume":"242","author":"Wallace","year":"1988","journal-title":"Science"},{"issue":"3","key":"2024043010124865500_fcae041-B3","doi-asserted-by":"crossref","first-page":"632","DOI":"10.3390\/jcm11030632","article-title":"Molecular genetics overview of primary mitochondrial myopathies","volume":"11","author":"Arena","year":"2022","journal-title":"J Clin Med"},{"issue":"10","key":"2024043010124865500_fcae041-B4","doi-asserted-by":"crossref","first-page":"978","DOI":"10.1016\/j.nmd.2021.08.005","article-title":"Primary mitochondrial myopathies in childhood","volume":"31","author":"Olimpio","year":"2021","journal-title":"Neuromuscul Disord"},{"issue":"8","key":"2024043010124865500_fcae041-B5","doi-asserted-by":"crossref","first-page":"429","DOI":"10.1038\/nrneurol.2013.126","article-title":"The clinical maze of mitochondrial neurology","volume":"9","author":"DiMauro","year":"2013","journal-title":"Nat Rev Neurol"},{"issue":"2","key":"2024043010124865500_fcae041-B6","doi-asserted-by":"crossref","first-page":"e402","DOI":"10.1212\/NXG.0000000000000402","article-title":"Mitochondrial diseases in North America: An analysis of the NAMDC registry","volume":"6","author":"Barca","year":"2020","journal-title":"Neurol Genet"},{"issue":"5","key":"2024043010124865500_fcae041-B7","doi-asserted-by":"crossref","first-page":"1301","DOI":"10.1007\/s00415-015-7710-y","article-title":"Redefining phenotypes associated with mitochondrial DNA single deletion","volume":"262","author":"Mancuso","year":"2015","journal-title":"J Neurol"},{"issue":"8","key":"2024043010124865500_fcae041-B8","doi-asserted-by":"crossref","first-page":"936","DOI":"10.1136\/jnnp-2012-303528","article-title":"The UK MRC Mitochondrial Disease Patient Cohort Study: Clinical phenotypes associated with the m.3243A&gt;G mutation\u2014Implications for diagnosis and management","volume":"84","author":"Nesbitt","year":"2013","journal-title":"J Neurol Neurosurg Psychiatry"},{"issue":"8","key":"2024043010124865500_fcae041-B9","doi-asserted-by":"crossref","first-page":"1777","DOI":"10.1007\/s00415-017-8567-z","article-title":"Revisiting mitochondrial ocular myopathies: A study from the Italian Network","volume":"264","author":"Orsucci","year":"2017","journal-title":"J Neurol"},{"issue":"Suppl 3(3-3)","key":"2024043010124865500_fcae041-B10","doi-asserted-by":"crossref","first-page":"S226","DOI":"10.1016\/j.nmd.2012.10.012","article-title":"Fatigue and exercise intolerance in mitochondrial diseases. 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