Study summary · research use only
Mitochondrial approaches for neuroprotection
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This review discusses mitochondrial approaches for neuroprotection (human and animal-model evidence). The authors state that evidence from postmortem brain tissue, genetic analysis, and biochemical and pathological studies in animal models suggests mitochondrial dysfunction is a common pathological mechanism in neurodegeneration, arising from oxidative stress, mitochondrial DNA deletions, mutations, altered morphology, and pathogenic protein interactions. They discuss potential therapeutic agents including creatine, coenzyme Q10, idebenone, synthetic triterpenoids, mitochondria-targeted antioxidants (MitoQ), and peptides (SS-31) in in vitro studies and animal models of Parkinson's, Huntington's, amyotrophic lateral sclerosis, and Alzheimer's disease. They review the status of clinical trials of creatine, coenzyme Q10, idebenone, and MitoQ, and note newly identified targets including a peroxisome proliferator-activated receptor-gamma coactivator and sirtuins. The review presents no new numerical results.
Abstract
A large body of evidence from postmortem brain tissue and genetic analysis in humans and biochemical and pathological studies in animal models (transgenic and toxin) of neurodegeneration suggest that mitochondrial dysfunction is a common pathological mechanism. Mitochondrial dysfunction from oxidative stress, mitochondrial DNA deletions, pathological mutations, altered mitochondrial morphology, and interaction of pathogenic proteins with mitochondria leads to neuronal demise. Therefore, therapeutic approaches targeting mitochondrial dysfunction and oxidative damage hold great promise in neurodegenerative diseases. This review discusses the potential therapeutic efficacy of creatine, coenzyme Q10, idebenone, synthetic triterpenoids, and mitochondrial targeted antioxidants (MitoQ) and peptides (SS-31) in in vitro studies and in animal models of Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, and Alzheimer's disease. We have also reviewed the current status of clinical trials of creatine, coenzyme Q10, idebenone, and MitoQ in neurodegenerative disorders. Further, we discuss newly identified therapeutic targets, including peroxisome proliferator-activated receptor-gamma-coactivator and sirtuins, which provide promise for future therapeutic developments in neurodegenerative disorders.
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