a UCLouvain team discovers the precision mechanics behind certain genetic forms

This discovery is magnificent precision mechanics at the level of our cells. The case takes place at the stage where our beautiful interior motorization transforms its fuel, sugar, into energy: the metabolization of sugar. What does it have to do with Parkinson’s disease? Patience, you’ll see, it’s exciting.

There was this gene, which everyone was talking about on a scientific level, and which, when it was inactivated, was responsible for certain forms of Parkinson’s disease. Everyone was talking about it, but how did it work? Almost everyone had their explanation. Which makes Professor Guido Bommer, head of the research team at the Duve Institute (UCLouvain), say with humor that this gene called PARK7 has already seen all kinds of things.

According to the publications, PARK7 did everything in life, except make coffee in the morning

On microscopic examination, Parkinson’s disease is characterized by a loss of neurons in a region located in the upper part of the brainstem, called “substantia nigra”. But why do these neurons die? “This Parkinson’s disease is quite enigmatic, eexplains Professor Guido Bommer, who conducted the research at the Duve Institute (UCLouvain). Because we have no idea why it develops in most patients. There are very few cases that are linked to changes in our genome. One of these changes is linked to a gene called PARK7.

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About this mysterious gene, “on was not happy with what was not understood“, continues Professor Bommer. When we started our research, there were already 1500 publications on this gene, but we found almost all the functions we could imagine at PARK7“. Except the one about the coffee machine, you’ve already read the joke.

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Frustrated at not understanding, the team said to themselves that it was not possible. It was necessary to know more about the enigmatic role of PARK7. “We said to ourselves, we must be simpler. Look for changes in tiny molecules that exist in our cells“.

This is how the research team from the Duve Institute (UCLouvain) found damage, damage at the level of metabolites, the small compounds necessary to bind our ingested nutrients and the energy absorbed in our cells.

A guardian has been found that prevents the damage that occurs due to sugar metabolism

Our brain needs sugar. He consumes 150 grams a day. Without sugar metabolism, the brain would not function. Evolution has found a way to prevent this metabolism from doing damage, thanks to PARK7, the guardian.

PARK7, the firefighter

This enzyme, possessed by all living beings, can destroy this reactive compound and prevent damage. It’s a bit like the fireman of the fire of our sugar metabolism. The research team was able to observe that it was enough to inactivate PARK7 to cause an accumulation of damage in human cells, mice or flies. She discovered a close link between sugar metabolism and this new type of cell damage that seems to play a role in some cases of Parkinson’s disease.

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The surprise“, says Professor Bommer, it was ultimately that the compound that forms when our cells take sugar and convert it step by step, into simpler things, extracting energy, damages both proteins and these small metabolites in the same way. When we metabolize sugar, there is always damage that is formed by a mechanism, which was once not known. What is extraordinary is that this damage is formed very little in our body, normally, because this PARK7 enzyme prevents the formation of this damage“Except when PARK7 is out of service… In other words, we knew about the failure of PARK7, in some Parkinsons, but we didn’t know how it damaged the engine.

Therapeutic prospects?

Parkinson’s disease affects approximately 40,000 Belgians. With the aging of the population, it is estimated that this number will double over the next 25 years. Each year, 2000 new cases are diagnosed in Belgium.

The average age of onset of this neurological, degenerative and progressive disease is between 50 and 55 years. But more than 10% of those affected develop the disease at an early stage (before age 40).

The hope for the future would be to develop treatments that would no longer just target the symptoms but the causes of the disease. We are still far from it.

The study was published in the American journal Proceedings of the National Academy of Sciences (PNAS). It was produced with the support of WELBIO and the European Research Council (ERC).


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