Methods for the treatment of mitochondrial disease
A mitochondrial and disease technology, applied in metabolic diseases, sensory diseases, disease diagnosis, etc., can solve the problem of no cure for mitochondria-based diseases, etc.
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Embodiment 1
[0227] Example 1: Confirmation of SURF1 Mutant Subjects
[0228] SURF1 mutations often produce profound complex IV defects. Monomeric complex IV is highly abnormal, showing reduced assembly and unusually high and low molecular weight complex IV structures ( figure 1 , Image 6 ). figure 1 Monomeric complex IV from pediatric and adult patients with Reye's disease is shown. Pediatric patients show reduced monomeric complex IV assembly with abnormal molecular weight forms of complex IV. These abnormal complex IV structures may represent abnormally assembled and dysfunctional complex IV. Image 6 Complex IV assembly is shown in two pediatric subjects with Reye's disease. Accordingly, subjects suffering from Reye's disease can be treated with the aromatic-cationic peptides disclosed herein.
Embodiment 2
[0229] Example 2: D-Arg-2',6'-Dmt-Lys-Phe-NH 2 (SS-31) Increased OXPHOS in SURF1 Mutations
[0230] SURF1 was mutated in two regions: 1) exon 4: 344-353del10, insAT (deleted sequence=TCTGCCAGCC) (heterozygous) and 2) exon 9: 875-876delCT (heterozygous). Fibroblasts were transformed with mutated SURF1.
[0231] Mutant SURF1-transformed cells were then grown in DMEM and divided into three groups. Group 1 (saline group) was treated with DMEM+saline. Group 2 (chronic treatment group) was treated with DMEM+10 nMSS-31 for 5 days. Group 3 (acute treatment group) was treated with DMEM+10 nMSS-31 for 1 day (16-24 hours). Untransformed fibroblasts were used as controls and divided into three treatment groups as listed above.
[0232] Transformed and control fibroblasts were also cultured under glycolysis inhibiting conditions. Under glycolysis-inhibited conditions, fibroblasts were cultured in glycolysis-inhibited medium supplemented with lactate and pyruvate. Conditions of...
Embodiment 3
[0240] Example 3: D-Arg-2',6'-Dmt-Lys-Phe-NH 2 Increased OXPHOS in POLG mutations
[0241] Fibroblasts transformed with the POLG mutant gene, a mutation at exon 7; c.13399G>A, p.Ala467Thr (homozygous). POLG encodes the catalytic subunit of DNA polymerase gamma, which is required for the replication and repair of mitochondrial DNA. Mutations in POLG are known to cause progressive external ophthalmoplegia (PEO), Alpers' disease, and sensory ataxic neuropathy with dysarthria and ophthalmoparesis (SANDO).
[0242] Mutant POLG fibroblasts were grown and divided into three groups. Group 1 (saline group) was treated with DMEM and saline. Group 2 (chronic treatment group) was treated with DMEM+10nMD-Arg-2',6'-Dmt-Lys-Phe-NH 2 Treat for 5 days. Group 3 (acute treatment group) was treated with DMEM+10nMD-Arg-2',6'-Dmt-Lys-Phe-NH 2 Treat for 1 day (16-24 hours). Untransformed fibroblasts were used as controls and divided into three treatment groups as listed above.
[0243]...
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