Mitochondria are the power plants of our cells — tiny “cell organs” that produce ATP, the universal cell fuel. As we age, more and more of our mitochondria become inoperable. They become less efficient at producing ATP and contribute to oxidative stress and inflammation. Scientists hope that many aspects of the aging process can be slowed down if ways are found to prevent or reverse mitochondrial dysfunction.

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There are various approaches to this, such as drugs that improve the cell's “mitochondrial quality control” and promote the breakdown of defective mitochondria. Another approach is to simply transplant mitochondria from young people into the cells of older people.

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In a recent study, 24 rats aged 22 months (equivalent to around 80 human years) were divided into four groups, with two groups receiving dummy treatment while the other two groups were injected with mitochondria isolated from the brains of young (3-month-old) rats. One of the untreated groups and one of the treated groups were exposed to mild stress one month before the injection. This included things like intermittent white noise and food deprivation for one day at a time.

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The researchers studied their brains by measuring levels of proteins associated with brain cell death and mitochondrial dysfunction. The main findings of this research:

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- Mitochondrial transplantation was associated with a significant reduction in neuron loss in the prefrontal cortex.

- Transplantation reduced markers of mitochondrial dysfunction.

- The transplant reduced brain damage caused by environmental stress.

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In older rats, regardless of whether they were exposed to stress or not, transplantation of mitochondria was associated with a significant decrease in proteins that promote apoptosis (self-destruction) of neurons in the prefrontal cortex and with a significant increase in proteins that suppress apoptosis. The researchers also found a decrease in cytochrome c, a molecule released by dysfunctional mitochondria.

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Harmful molecules produced by mitochondria can damage cells and tissues through a process known as oxidative stress. The brain may be particularly vulnerable to oxidative stress, and environmental stressors may cause increased oxidative stress in the brain. When measuring the oxidative stress marker MDA (malondialdehyde) in the prefrontal cortex, the researchers found that environmental stressors significantly increased MDA levels, while this effect was attenuated in rats that were given young mitochondria.

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These results suggest that mitochondrial transplantation could be an effective way to slow down the death of nerve cells due to aging and the environment, and that this is worth investigating in humans. However, this method is not as exciting and practical as some other approaches that are currently being developed. The biggest challenge would be finding out how to produce large quantities of human mitochondria. A more sustainable solution would be to move the genetic material in the mitochondria to the cell nucleus, where it would be better protected against damage. But there is probably still a long way to go until then.