Mitochondria, the swarming power plants of the cell, become damaged and dysfunctional with age. Can this be addressed by delivering complete, whole, new mitochondria as a therapy? There have been signs in past years that cells can ingest and incorporate mitochondria from the surrounding environment, but few useful demonstrations to show whether or not this is common in living tissues. In the research here, researchers achieve that result, delivering mitochondria into tissues as a therapy, and using this approach to treat an animal model of Parkinson’s disease. This neurodegenerative condition is associated with degraded mitochondrial function, especially in the dopamine-generating neurons in the brain; depletion of that cell population produces the visible symptoms of the disease.

Unfortunately it isn’t clear as to whether usefulness in addressing mitochondrial dysfunction in Parkinson’s will translate to usefulness in addressing the type of mitochondrial dysfunction thought to cause aging in general. The contribution to aging is based on damage to mitochondrial DNA resulting in mutant mitochondria that are both malfunctioning and capable of outcompeting the normal mitochondria present in a cell quite quickly. Delivering new, fully functional mitochondria might not do much in this situation; they would simply be outcompeted again. It still seems worth the attempt if it turns out to be comparatively easy to replicate this demonstration in mice, on the grounds that you never know in certainty until you try, but I’m not optimistic based on the current understanding of the situation. On the other hand, one potentially interesting application of mitochondrial uptake might be to provide people an upgrade from a comparatively poor mitochondrial haplotype to a comparatively better mitochondrial haplotype, as different mitochondrial genomes have different performance characteristics.

Mitochondrial dysfunction is associated with a large number of human diseases, including neurological and muscular degeneration, cardiovascular disorders, obesity, diabetes, aging and rare mitochondrial diseases. Replacement of dysfunctional mitochondria with functional exogenous mitochondria is proposed as a general principle to treat these diseases. Here we found that mitochondria isolated from human hepatoma cell could naturally enter human neuroblastoma cell line, and when the mitochondria were intravenously injected into mice, all of the mice were survived and no obvious abnormality appeared. The results of in vivo distribution suggested that the exogenous mitochondria distributed in various tissues including brain, liver, kidney, muscle and heart, which would benefit for multi-systemically mitochondrial diseases.

In normal mice, mitochondrial supplement improved their endurance by increase of energy production in forced swimming test; and in experimental Parkinson’s disease (PD) model mice induced by respiratory chain inhibitor MPTP, mitochondrial replacement prevented experimental PD progress through increasing the activity of electron transport chain, decreasing reactive oxygen species level, and preventing cell apoptosis and necrosis. Since effective drugs remain elusive to date for mitochondrial diseases, the strategy of mitochondrial replacement would provide an essential and innovative approach as mitochondrial therapy.


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