ArticleTranslational medicine of aging2020
Mitochondrial hyperactivity as a potential therapeutic target in Parkinson's disease.
Article in Translational medicine of aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Quercetin Impairs the Growth of Uveal Melanoma Cells by Interfering with Glucose Uptake and Metabolism.International journal of molecular sciences · 2024Article
- Neuronal cell cycle reentry events in the aging brain are more prevalent in neurodegeneration and lead to cellular senescence.PLoS biology · 2024Article
- Gut-to-Brain α-Synuclein Transmission in Parkinson's Disease: Evidence for Prion-like Mechanisms.International journal of molecular sciences · 2023Review
- GAIT-GM integrative cross-omics analyses reveal cholinergic defects in a C. elegans model of Parkinson's disease.Scientific reports · 2022Article
- Synergistic Effects of Milk-Derived Exosomes and Galactose onInternational journal of molecular sciences · 2021Review
- Directly Reprogrammed Human Neurons to Understand Age-Related Energy Metabolism Impairment and Mitochondrial Dysfunction in Healthy Aging and Neurodegeneration.Oxidative medicine and cellular longevity · 2021Review
- Introduction: Special issue on Aging Science Talks: Science for our community during isolation.Translational medicine of aging · 2020Article
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
Mitochondrial dysfunction is thought to contribute to neurodegeneration in Parkinson's disease (PD), yet the cellular events that lead to mitochondrial disruption remain unclear. Post-mortem studies of PD patient brains and the use of complex I inhibitors to model the disease previously suggested a reduction in mitochondrial activity as a causative factor in PD, but this may represent an endpoint in the disease process. In our recent studies, we identified a novel link between branched-chain amino acid metabolism and PD, and uncovered mitochondrial hyperactivity as a potential alternative mechanism of PD pathogenesis. Increased mitochondrial activity may occur in a subset of PD patients, or may be a more common early event that precedes the ultimate loss of mitochondrial function. Therefore, it may be that any imbalance in mitochondrial activity, either increased or decreased, could cause a loss of mitochondrial homeostasis that leads to disease. An effective therapeutic strategy may be to target specific imbalances in activity at selective stages of PD or in specific patients, with any efforts to reduce mitochondrial activity constituting a surprising new avenue for PD treatment.
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