Investigating Parkinson’s as an autoimmune disease

Louis-Eric Trudeau
Professor
University of Montreal

At the University of Montreal, Professor Louis-Eric Trudeau investigates the earliest potential causes of Parkinson’s disease, at the cellular level. His project is funded by the Saucier-van Berkom Parkinson Quebec Research Fund with contributions from Parkinson Newfoundland & Labrador, in the amount of $49,748.00 for 1 year. He is exploring the possibility that Parkinson’s is a form of autoimmune disease, caused when the immune system attacks the axon terminals in our brain cells. Those extremities release the chemical messengers that communicate with other cells, and damage to such terminals may disrupt the dopamine-producing brain cells that are key to Parkinson’s. 

The death of the brain cells that produce dopamine, the chemical messenger that signals other cells involved in motor control, triggers the symptoms of Parkinson’s disease. But researchers still don’t know exactly what causes those dopamine-producing cells to die.

Trudeau, a neuroscientist, investigates the possibility that an autoimmune attack on those dopamine cells is the culprit.

Trudeau and his immunologist colleague, Michel Desjardins, are studying the role of the portion of cells called axon terminals. These terminals—the root-like extremities of cells—release the chemical messengers that send communication signals. Trudeau believes the death of these terminals, before the death of the dopamine cells themselves, is where the trouble starts.

Using dopamine-producing brain cells from genetically modified mice, Trudeau and his team are exposing dopamine cells directly to immune cells. Then they closely study the axon terminals of those dopamine cells to see what happens in an immune attack.  

“This project is focused on trying to develop a better understanding of why the terminals are affected,” Trudeau says. “This is a relatively new field in Parkinson’s disease looking at the possibility that this disease is at least in part an autoimmune disease, in some ways like Multiple Sclerosis (MS).”

If Trudeau and his colleagues demonstrate that the axon terminals are a critical site that an autoimmune process attacks, that knowledge could help researchers devise a way to stop the immune reaction.

“If we can intervene and stop the immune reaction it may be possible to prevent further loss of dopamine-producing cells,” Trudeau says.

Drug companies are already developing new drugs to treat MS and other autoimmune disorders by influencing the immune system, but they have not so far been considering them for Parkinson’s disease. If Trudeau and his colleagues’ work is ultimately successful, it would open up a new avenue to apply these or similar drugs to stop the immune cells’ attack of these key brain cells.

“The immune system can be relatively easily targeted for treatment,” Trudeau says.

Although Trudeau initially pursued a bachelor’s degree in psychology, he soon realized he was more interested in how disturbances in the brain’s basic functioning lead to disease. For the last 20 years, his lab has studied the basic function of dopamine-producing brain cells—leading to his research into Parkinson’s disease.

“It’s very clear that the reason we don’t have many good treatments for diseases of the brain like Parkinson’s is because our understanding of how the brain does its normal functions is not developed enough,” he says.   “Axon terminals are really where a lot of the action is. This is where dopamine is released in the brain and this is what you want to preserve if you want to preserve function and prevent the motor symptoms (of Parkinson’s) from appearing or progressing.”

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