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Scientists at the La Jolla Institute for Immunology (LJI) found that people with Parkinson’s disease have a clear “genetic signature” of the disease in their memory T cells. Scientists hope that working with these genes could open the door to new treatments and diagnoses for Parkinson’s.
“Parkinson’s disease is not generally considered an autoimmune disease,” says Cecilia Lindestam Arlehamn of La Jolla (LJI). “But all of our work points to a role for T cells in the disease.”
“Now that we can see what these T cells do, we think that intervening with antibody therapies could have an impact on disease progression, especially early on,” adds LJI Professor Alessandro Sette, who led the work with Lindestam. Arlehamn.
This study was recently published in the journal «Npj Parkinson’s Disease».
Parkinson’s progresses as dopamine-producing neurons in the brain die. Unfortunately, scientists have not been able to identify what causes this cell deathalthough they have a clue: damaged neurons contain clumps of a damaged protein called alpha-sinuclein.
LJI’s research suggests that these clusters may be the kiss of death for dopamine-producing neurons. Sette and Arlehamn recently showed that people with Parkinson’s have T cells that target alpha-synuclein early in Parkinson’s disease.
Autoreactive T cells can damage the body’s own cells, including neurons. In fact, autoreactive T cells are to blame for many autoimmune diseases.
The new study offers a way to stop these T cells in their tracks. The LJI team found that people with Parkinson’s disease have memory T cells with a very specific genetic signature. These genes seem to be responsible to attack alpha-synuclein and potentially cause ongoing inflammation in Parkinson’s.
“The identification of these genes will make it possible to see which patients have T cells that respond to alpha-synuclein and which do not,” says the researcher.
An important gene expressed on these T cells is LRRK2. This gene is associated with the genetic or familial type of Parkinson’s disease. Neurons in many people with Parkinson’s express LRRK2, but the new study is the first to show this gene expressed in T cells.
But many of the genes expressed in these T cells were completely unexpected and were not previously related to Parkinson’s disease. “This finding suggests that we find new targets for potential therapies,” adds Sette.
In the future, Arlehamn and his collaborators plan to study post-mortem brain samples. This work will confirm whether the same autoreactive T cells found in the blood also target neurons in people with Parkinson’s. The team also wants to search other targets, called antigenswhich can be recognized by T cells in people with Parkinson’s disease.
To translate this work into new therapies, it will be important for scientists to study how they can activate or inhibit different genes at stages of Parkinson’s progression.
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