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Longevity Briefs: Can Young Mitochondria Help Protect Old Brains?

Posted on 20 June 2023

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Longevity briefs provides a short summary of novel research in biology, medicine, or biotechnology that caught the attention of our researchers in Oxford, due to its potential to improve our health, wellbeing, and longevity.

Why is this research important: The mitochondria are the power plants of our cells – tiny ‘cellular organs’ that generate ATP, the universal cellular fuel. As we age, an increasing number of our mitochondria become dysfunctional. They get less efficient at producing ATP, and they also contribute to oxidative stress and inflammation. Scientists hope that by discovering ways to prevent or reverse mitochondrial dysfunction, we may be able to slow many aspects of the ageing process.

Depictions of a healthy (left) and dysfunctional (right) mitochondria.
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There are various approaches to this, such as drugs that improve the ‘mitochondrial quality control’ of the cell, encouraging the destruction of faulty mitochondria. Another approach is to simply transplant mitochondria from young people into the cells of older people. Cells will absorb mitochondria from their surroundings and make use of them unprompted.

What did the researchers do: In this study, researchers took 24 rats aged 22 months old (roughly equivalent to 80 ‘human years’) and divided them into four groups. Two groups then received a sham treatment, while the other two received an injection of mitochondria isolated from the brains of young (3 month old) rats. These mitochondria were injected into the cerebral ventricles in the brain (which contain cerebrospinal fluid). One of the untreated groups and one of the treated groups were also exposed to mild forms of stress during the month prior to the injection. These included things like intermittent white noise and depriving the rats of food for a day at a time.

Two days later, the rats were sacrificed and researchers studied their brains by measuring levels of proteins linked to brain cell death and mitochondrial dysfunction.

Key takeaway(s) from this research:

  • Mitochondrial transplantation was associated with a significant reduction in neuron death in the prefrontal cortex.
  • Transplantation reduced markers of mitochondrial dysfunction.
  • Transplantation alleviated damage in the brain related to environmental stress.

In elderly rats, whether exposed to stress or not, mitochondrial transplantation was associated with a significant reduction in proteins that promote apoptosis (self-destruction) of neurons in the prefrontal cortex, and a significant increase in proteins that suppress apoptosis. Researchers also detected a reduction in cytochrome c, a molecule that is released from dysfunctional mitochondria.

Harmful molecules generated by mitochondria can damage cells and tissues in a process called oxidative stress. The brain may be particularly sensitive to oxidative stress, and environmental stressors can generate increased oxidative stress in the brain. When the researchers measured a marker of oxidative stress called MDA (malondialdehyde) in the prefrontal cortex, they found that environmental stressors significantly increased MDA levels, but this was alleviated in rats treated who had received young mitochondria.

These results suggest that mitochondrial transplantation could be an effective way of reducing neuronal death related to ageing and environmental stress, and is worth exploring in humans. It’s not quite as exciting or as practical as some of the other approaches under development, though. The main challenge would be figuring out how to produce large quantities of human mitochondria. A more permanent solution would be to relocate the genetic material in the mitochondria to the nucleus of the cell, where it would be better protected from damage. That’s likely to be a long way off, however.

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    Chronic stress-induced apoptosis is mitigated by young mitochondria transplantation in the prefrontal cortex of aged rats

    Title image generated by DALL.E

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