T3 increases mitochondrial oxidative phosphorylation. This has huge impacts on which hypothyroidism is currently managed (only evaluate TSH and T4) and disease implication. We know that decoupling of oxidative phosporylation and a shift to glycolysis and glutaminolysis (substrate-level phosphorylation) results in genomic mutability and cancer, then a low T3 has implications in cancer prevention
T3 induces beneficial oxidative changes in muscles through its interaction with mitochondrial receptors. PGC-1alpha and PPAR-gamma were involved in this process. The important point here is that T3 is increasing oxidative function of muscle through interaction with mitochondria.
Bioidentical progesterone shown to reduce post TBI mitochondrial dysfunction. This has significant implications on the ability of the damaged brain to heal and recover, thus limiting post-injury cognitive deficits.
Huperzine A, a natural acetylcholinesterase inhibitor, provides neuroprotection through increase mitochondrial function and decrease in accumulated amyloid Beta protein.
mitochondrial dysfunction has a central role in the pathogenesis of Alzheimer's, Parkinson's and Huntington's diseases and amyotrophic lateral sclerosis
mitochondrial dysfunction has a central role in the pathogenesis of Alzheimer's, Parkinson's and Huntington's diseases and amyotrophic lateral sclerosis
Discussion of the mitochondrial role in chronic fatigue syndrome. As the authors conclude, there is dysfunction, but whether the cause is primary or secondary or likely varies from individual to individual is yet undetermined.