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Does our immune response affect the risk of developing Parkinson’s disease?

An illustration showing a rat injected with alpha-synuclein. A zoomed in circle displays immune cells in the brain.
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T-cells, antibodies, and antigens. During the past year, we have learned a lot about our immune system through media. Most people agree that the immune system is crucial for our survival. But how does the immune system affect Parkinson’s disease; is it necessary to keep our brains healthy, or does it contribute to disease progression? The answer to that question is unfortunately not straightforward.

Filip Bäckström is a doctoral student at the Faculty of Medicine, Lund University. Here he tells us about his research.

Genetic variation is the reason why we are different, some have blue eyes and others brown, some are tall whereas others are short. Genetic variation also affects our immune system. The involvement of the immune system in Parkinson’s disease has been known for some time now. However, even after decades of research, there is still a debate regarding its protective or detrimental effects on disease progression. Our aim is to answer the question: how does the genetic variation in our immune system affect the risk and progression of Parkinson’s disease?

To study the effects of the immune system on the brain, we use rats that are identical in their genetic background except for a gene involved in immune responses. Since rats do not develop Parkinson’s disease, we have to mimic the disease (described below). We have found that genetic differences in the immune system affect how many immune cells are present in the brain, how strongly these cells become activated, and the number of brain cells that die in the disease. However, we still do not know how the immune cells outside the brain react to or contribute to the disease.  This is something that we are investigating at the moment.

By studying how genetic differences in the immune system affect brain pathology in rats, we aim to identify biological processes that could be targeted for future treatment of Parkinson’s disease.

How you can mimic Parkinson’s disease in rats

Alpha-synuclein is a protein that is present in all of us. In patients with Parkinson’s disease, this protein clumps together in certain brain cells. This is believed to be a contributing cause for the subsequent death of these cells.

By two injections into the brain of rats we can, to some degree, mimic Parkinson’s disease.

First, we inject a virus that produces large amounts of alpha-synuclein. Next, we inject alpha-synuclein that has already clumped together. These two injections result in a progressive process of more and more protein clumping together, a process that resembles what happens in patients with Parkinson’s disease. In this way, we are able to study how the immune system reacts to and affects the progression of Parkinson’s disease in living organisms.

Profile photo of Filip Bäckström.

Filip Bäckström

Ph.D. student at Translational Neurogenetics and  Clinical Neurophysiology

filip [dot] backstrom [at] med [dot] lu [dot] se 

Link to Filip Bäckström's profile in the LU Research Portal.