Researchers in Germany have found further evidence to support the idea that Parkinson's could be an autoimmune disease.
Dopamine is a chemical messenger that supports many important brain functions. These include functions that deal with reward, emotions, pleasure, and movement control.
In Parkinson's disease, the midbrain neurons, or brain cells, that make dopamine die off. But it is not clear what causes their death.
As more and more dopamine cells die, levels of the chemical messenger drop, giving rise to symptoms such as tremor, slowness, rigidity, and problems with balance. Problems with speech and swallowing also develop, as do several nonmovement symptoms.
Estimates suggest that around half a million people in the United States have Parkinson's disease.
Autoimmunity and Parkinson's
Autoimmune diseases arise because the immune system attacks healthy organs, tissues, and cells instead of protecting them.
Although the idea that Parkinson's could be an autoimmune disease is not new, the biological evidence to back it up is only just emerging.
In 2017, for instance, a study from the U.S. revealed how pieces of a protein that builds up in the dopamine cells of people with Parkinson's can trigger a deadly immune attack against the cells.
More recently, scientists have linked the use of drugs that subdue the immune system to a lower risk of developing Parkinson's disease.
In the new study, researchers from Friedrich-Alexander-Universität (FAU) in Erlangen-Nürnberg, Germany, have shown that T helper 17 (Th17) cells — a type of immune T cell — attack dopamine cells derived from people with Parkinson's disease but not those derived from people without it.
They report their findings in the journal Cell Stem Cell.
"Thanks to our investigations," says senior study author Beate Winner, a professor in the Department of Stem Cell Biology at FAU, "we were able to clearly prove not only that [T cells] are involved in causing Parkinson's disease, but also what role they actually play."
Stem cell model of Parkinson's disease
Together with a team from the movement disorders clinic at University Hospital Erlangen, the FAU researchers had earlier discovered that the brains of those with Parkinson's had higher levels of Th17 cells.
Th17 cells are also found in higher amounts in people with rheumatoid arthritis and other autoimmune diseases.
The discovery spurred the team to investigate further using a stem cell model of Parkinson's disease.
To develop the model, they took skin cells from people with and without Parkinson's and induced them to become "pluripotent stem cells." Pluripotent stem cells have the ability to mature into virtually any type of cell, including neurons.
They coaxed the stem cells to mature into midbrain neurons that make dopamine. This meant that they had batches of newly created dopamine cells that were specific to each of the patients.
The team then exposed each batch of dopamine cells to fresh Th17 cells taken from the patients. In this way, each batch of patient-specific dopamine cells was exposed only to Th17 cells that came from that same patient.
The results showed that while the Th17 cells killed many of the dopamine cells from patients with Parkinson's, this did not happen with the cells that came from patients without the disease.
In further experiments, the scientists also discovered that an antibody that was already in use in the hospital for the treatment of psoriasis was "able to largely prevent the death" of the brain cells.
"The findings from our study offer a significant basis for new methods of treating Parkinson's disease."
Prof. Beate Winner