A growing number of scientists around the world are trying to find new ways to improve the health of the cells in the body. This line of research could help provide treatments for people with long Covid, as well as revolutionising our understanding of everything from Parkinson's disease to the aging process.
Mitochondria, tiny tube-shaped structures that are found in their hundreds, sometimes thousands, in nearly all of our cells, are known as the body's power plants and act as a form of energy currency for cells. Our organs would grind to a halt if we didn't have the fuel we need to function.
One of the complexities of mitochondria is that they have their own DNA, separate from the DNA stored in the nuclei of our cells
Scientists have found that mitochondria do more than just generate a certain amount of energy. They can help keep us warm when we are cold by using an alternative form of heat generation, and studies have shown that the mitochondria in the eye play a role in helping us see.
The more we look, the more we discover that they contribute to the many building blocks of life that keep us healthy. The natural process of cell death that occurs over and over again throughout our lives is the result of old and damaged cells being identified and destroyed.
They are vital to our survival, but we only notice when they go wrong. Mitochondria are involved in many processes so when they don't function well, this can lead to diseases.
One of the unique features of mitochondria is that they have their own genetic material, which is different from what is in the nucleus of our cells. Mitochondrial DNA consists of less than 17,000 base pairs and is passed down from mother to child. Over the past decade, scientists have found that a variety of chronic illnesses can be traced back to the fact that mtDNA can be damaged by certain types of infections.
Mitochondrial diseases are caused by genetic defects. The consequences are grave if they affect one in 4,300 people. Most patients will live between 10 and 35 years, with most dying from general body wasting due to brain or muscle damage, or impairments to the heart and kidneys. Minczuk has a research group at the University of Cambridge that is interested in the role that mtDNA can play in Parkinson's.
Some Parkinson's patients have genes that prevent damaged mitochondria being eliminated and replaced with healthy ones. As a result, the existing mitochondria in the body accumulate more and more mutations, with damaging consequences for cells that depend on the energy they supply.
The rise of new gene-editing techniques may lead to new treatment solutions for a variety of diseases in the future. This has been a challenge because Crispr technology can't be used to tinker with the mtDNA, as it isn't possible to deliver RNA into it.
Over the past few years, scientists like Minczuk have designed enzymes that can achieve the same effect as Crispr. Future potential is offered by studies on rodents.
Minczuk says that they are slowly gathering the tools to be able to modify the mitochondria. We want to be able to change the genetic make-up of mitochondria, but we also want to be able to change the genetic make-up of other parts of the body. We could study Parkinson's in much more detail. In order to see what happens, we could take a healthy mouse and modify it to have Parkinson's-like symptoms. The start of symptoms would be triggered by that.
Millions of people with long Covid and chronic fatigue syndrome, also known as ME/CFS, could be helped by finding more immediate ways to improve their mitochondria health.
A clinical trial is being run at Oxford University to see if a cocktail made by a Massachusetts-based company can help patients with chronic fatigue syndrome.
She hopes that the drug will help people with their energy levels and fatigue. The idea is that it can help repair damaged mitochondria. The results should be reported by the end of July.
Some patients with long Covid who find themselves exhausted by exercise after Covid-19 may be affected by the effects of the mitochondria. People with genetic mitochondrial diseases can also experience this symptom.
The muscles of long Covid patients with PEM struggle to extract oxygen from the blood as efficiently as might be expected. She concluded that the root cause was the fact that white blood cells weren't as efficient in generating ATP as they could have been.
The patients' mitochondria become sluggish in generating energy. A doctor at a Boston hospital believes he has found a cure for ME/CFS through studying patients with the illness, which is often caused by viral infections.
After studying the mitochondrial DNA of these patients, it appeared to be normal, but after taking a deep look at the electron level in the mitochondria, he was able to identify a problem.
In both ME/CFS and long Covid, it is most likely that these are acquired forms of mitochondria damage, which is related to the initial infections or an immune response. The inability of the mitochondria to serve the needs of the muscles is caused by this.
Both ME/CFS and long Covid patients are being tested on a drug that aims to restore normal metabolism.
The two agree that a subset of long Covid and ME/CFS patients are likely to have a factor in their mitochondria function. The wide range of different symptoms that patients tend to report could be a result of the damage inflicted to the mitochondria.
When people with long Covid and ME/CFS try to do physical activity, they experience a rapid increase in heartbeat and lightheadedness. Damage to small sensory nerves in the skin is one of the reasons why this happens.
She says there is a possibility that the problem with the mitochondria may be first. Nerves are high energy tissues and dependent on normal mitochondrial function.
Different cell types have different numbers of mitochondria due to the different energy requirements. Organs with high energy demands such as the brain, the heart and the pancreas tend to have more, which has been linked to everything from cancer to type 2 diabetes.
Mitochondria are not the main factor in any of these diseases, but they are thought to be a key factor. The majority of heart failure is thought to be caused by a malfunction of the heart's mitochondria. The heart is dependent on continuous oxygen supply and can be affected by a number of risk factors.
When you get down to the cellular level, there are some surprising overlaps between exercise and disease, at least in the muscles
Mitochondrial drugs may have applications in other illnesses if they prove effective in Covid and ME/CFS, as well as to understand how the aging process affects our cells.
Scientists are looking for ways to improve the health of the cells in the body. Chris is looking at what we can learn from elite athletes to help those with muscle diseases and age related sarcopenia.
endurance runners have high numbers of extra- efficient mitochondria which form extensive networks throughout their muscle tissues to deal with the stresses of long-term exercise. It's possible to help people with diseases and keep them healthy in old age by understanding the pathways that lead to the adaptation of mitochondria. Clinical trials have shown that a supplement called urolithin A improves the health of older adults.
There are some surprising overlaps between exercise and disease in the muscles when you reach the cellular level. Exercise causes a lot of cellular stress. It depletes ATP reserves, it causes physical strain on the cell, and it acidifies the muscle cells, which is what happens in diseases.
Studies have shown that exercise can improve the health of older adults who lead sedentary lifestyles because of the way their mitochondria clusters together.
Adaptability is the basis of life. Exercise exposes our cells to different stressors which cause them to kick into action and regulate the situation. It is more efficient when we exercise again. As a result of that stress, you begin to build those capacities.
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