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Parkinson's partly an autoimmune disease?
Parkinson's is a neurodegenerative disease that is widespread throughout the world. Researchers have now found the first direct evidence that autoimmunity plays an important role in Parkinson's disease.
Columbia University Medical Center researchers (CUMC) found that autoimmunity has a strong influence on Parkinson's disease. If the immune system attacks the body's own tissue, this can have a significant impact on the development of Parkinson's. The physicians published the results of their study in the journal "Nature"
Our body's immune response seems to be involved in Parkinson's disease. A faulty immune system attack on neurons can be triggered if they have already been damaged by Parkinson's. (Image: Astrid Gast - fotolia) Alpha-synuclein can activate T-cells
The current research results show a way to prevent the death of neurons in Parkinson's disease by an immune response-dampening therapy, say the experts. The idea that a faulty immune system contributes to Parkinson's is almost 100 years old, explains author Professor David Sulzer. So far, however, no one was able to prove a connection. Our results show that two fragments of alpha-synuclein, a protein that accumulates in the brain cells of people with Parkinson's, can activate T cells, the researchers explain. These cells are involved in so-called autoimmune attacks.
Identify individuals at increased risk
It remains to be seen whether the immune response to alpha-synuclein is an initial cause of Parkinson's disease or whether it contributes to neuronal death and thus worsens the symptoms after the onset of the disease, explains author Professor Alessandro Sette. However, the current findings may help to develop a much-needed diagnostic test for Parkinson's disease and thus help identify those at high risk or affected in the early stages of the disease, the researchers explain.
T cells can view Alzheimer's damaged neurons as invaders
A 2014 study revealed that dopamine neurons (which are affected by Parkinson's disease) are particularly vulnerable because they have cell surface proteins that help the immune system detect foreign substances, the researchers explain. In other words, T-cells may view neurons as invaders foreign to the body if they have been damaged by Parkinson's disease.
Physicians examined more than 100 subjects for their study
In their study, the researchers examined the blood samples of 67 Parkinson's patients and 36 age-matched healthy volunteers. They searched for fragments of alpha-synuclein and other proteins that can be found in neurons. They analyzed the participants' samples to find out which protein fragments triggered an immune response.
What causes autoimmune response in Parkinson's disease?
The detected immune response was associated with the common form of a particular gene. This could explain why many people with Parkinson's disease carry such a gene variant, the scientists emphasize. The autoimmune response to Parkinson's disease arises when neurons are no longer able to break down the abnormal alpha synuclein, researchers suggest.
Recycling process of proteins is reduced by Parkinson's
Usually, the damaged proteins are broken down and recycled. However, this recycling process is decreasing with age and certain diseases - including Parkinson's, says Professor Sulzer in a Columbia University Medical Center press release.
Further research is needed
When the abnormal alpha-synuclein begins to accumulate, the immune system might confuse the protein with pathogens. This then leads to an attack by the immune system, explain the physicians. Additional research will now investigate the immune response in other patients and identify the molecular steps that lead to an autoimmune response in animal and cell models.
Immunotherapy could increase tolerance of the immune system for alpha-synuclein
The new findings open the possibility to use an immunotherapy approach to increase the tolerance of the immune system to alpha-synuclein. This may help to curb the worsening of symptoms in Parkinson's patients, adds Professor Sette. (As)