🧠 Parkinson's disease: one protein in particular could play a key role

For more than 50 years, Parkinson's disease has been associated with a loss of dopamine, a neurotransmitter essential for motor control. A study conducted at Laval University suggests that a transformation of the brain protein parkin could contribute to this loss and play an important role in the progression of the pathology. This discovery offers a new avenue for the development of treatments.

In a healthy person, parkin plays an important role in cleaning cells by helping to eliminate waste. In the brains of affected individuals, however, this protein appears to adopt an abnormal form that prevents it from fulfilling its function. Waste would then accumulate, which could lead to the death of dopaminergic neurons responsible for producing dopamine.


This abnormal form of parkin is insoluble—meaning it no longer dissolves normally in cells and tends to cluster into large aggregates. "The higher the ratio of aggregated parkin, the greater the loss of dopamine," explains Frédéric Calon, professor at the Faculty of Pharmacy and researcher at the CHU de Québec - Laval University Research Centre, who led the study. The transformation of the protein would also be linked to disease progression. "The longer the disease lasts, the more we observe the phenomenon," he adds.

In animal models where a loss of dopamine was artificially induced, parkin did not form these aggregates. This result supports the hypothesis that the transformation of the protein is not a consequence of the disease, but rather plays an early role in its development.

A key region

Even though parkin is found elsewhere in the brain, its transformation only occurs in the substantia nigra, a region in the center of the brain that is heavily involved in motor function. "It's a bit like an on/off system," illustrates the researcher. "When the substantia nigra works, movements are possible. When it stops working, they become very difficult."

The substantia nigra contains few dopaminergic neurons, but these are very active and particularly vulnerable. Their loss leads to the main motor symptoms of the disease, such as difficulty initiating movements or tremors at rest.

Studying this region remains a challenge because it is small and difficult to observe. To achieve this, the team collaborated with scientists from the University of Saskatchewan, who have a brain bank from people with Parkinson's disease at different stages. "It's really worth looking directly into people's brains. We have some who have had the disease for up to 20 years, and others around 5 years," says Professor Calon, whose study is supported by Parkinson Canada.

The team's work focused on observing this phenomenon, but further research will be needed to understand the mechanisms. Eventually, better understanding this transformation could open the door to new therapeutic approaches. "We could try to reverse the process to protect dopaminergic neurons," concludes Frédéric Calon.