Published on : 10 December 20214 min reading time
Parkinson’s disease may be the result of cell exhaustion
This process is the finding of a new study conducted by the University of Montreal in Canada and published in the journal Current Biology. The first author of the paper is Louis-Éric Trudeau, a professor of pharmacology and neuroscience, who has spent the past 17 years studying the part of the brain involved in the development of Parkinson’s disease, schizophrenia and addiction.
According to Trudeau, “Like an engine that is constantly running at full speed, these nerve cells have to produce an incredible amount of energy all the time to function. It seems that they overload themselves and die prematurely as a result.”
He hopes this knowledge will allow him to better simulate Parkinson’s disease in animal models and pave the way for new therapeutic approaches. Trudeau notes that it is currently extremely difficult to reproduce the symptoms of the disease in mice – even if human genes are inserted into the mouse genome.
With the new discoveries and associated opportunities, new drugs could be developed to help these brain cells reduce their energy consumption or make their energy conversion more efficient. This would reduce the damage to cells that occurs during the energy process. This is an idea that the research group is already actively pursuing.
Parkinson’s disease is pathophysiologically based on the destruction of brain cells in specific regions of the brain, such as the substantia nigra. Nerve cells affected by the disease physiologically release the neurotransmitter dopamine – a transmitter that regulates movement, emotional responses and other functions in humans.
As the disease progresses, the production and release of dopamine ceases. As a result, more and more symptoms such as tremors, bradykinesia, rigidity and postural instability appear. Symptoms that severely restrict the patient and make it increasingly difficult to walk, talk, eat or lead a normal life in general.
Mitochondria are stressed to the point of collapse
For the past 3 years, the team has been studying why mitochondria in brain regions affected by Parkinson’s disease work so intensely and therefore overheat. In a way, mitochondria are the power plants of our cells. They produce all the energy the cell needs to grow, to perform its functions and to trigger signals.
In the course of their work, the researchers noticed that the cells in the affected brain regions have a very complex structure. They have many extensions and sites where neurotransmitters can be released. The team suspects that this complexity is the reason why the cells have such a high energy requirement.
Trudeau says his findings support the idea that these highly complex neurons are running their mitochondria at a level far too high to meet their enormous energy needs. This theory would explain the accelerated decay of the cells.
Trudeau explains, “To stick with the engine example: a car that overheats uses a lot more fuel and, not surprisingly, ends up in the shop more often.
As we age, the complex structure of cells seems to be increasingly fatal to them, as it can make them more vulnerable – they are more likely to malfunction and die sooner. A mechanism that can then eventually trigger Parkinson’s disease, a disease of old age.
As life expectancy in this region increases, so does the need for new treatment methods for neurodegenerative diseases like Parkinson’s. Trudeau explains:
“From an evolutionary standpoint, some of our neurons may simply not be designed to function for 80, 90 or even 100 years. We have to assume that some parts of our body are less able than others to withstand the effects of time.
However, since only a very small part of the brain is affected by Parkinson’s disease, he remains hopeful that a new and effective treatment method will be found as soon as possible.