Autoimmune Parkinson's disease
Researchers at Columbia University and the Institute of Allergy and Immunology in La Jolla have received evidence that autoimmune reactions, in which the immune system affects the body's own tissues, contribute to the development of Parkinson's disease - one of the most common age–related neurodegenerative diseases. The data obtained by them indicate that the death of neurons in this disease can be prevented with the help of drugs that suppress immune responses.
According to one of the leaders of the study, Professor David Sulzer, the assumption that disorders in the immune system contribute to the development of Parkinson's disease has been made almost 100 years ago. However, until now, no one has been able to make a complete picture.
Until recently, it was assumed that neurons are protected from autoimmune reactions. However, in 2014, the authors demonstrated that dopamine neurons that die in Parkinson's disease are susceptible to the destructive effects of autoimmune processes, since they carry proteins on their surface that help the immune system recognize foreign substances. Based on the data obtained, they concluded that T-lymphocytes are capable of mistaking neurons damaged in Parkinson's disease for foreign agents.
In their new work, they found that T-lymphocytes recognize damaged dopamine neurons as foreign material due to the accumulation of damaged alpha-synuclein protein molecules in them, which is a key sign of Parkinson's disease. Professor Sulzer explains that in most cases of Parkinson's disease, a large number of Levi's bodies accumulate inside dopamine neurons, the main component of which is alpha-synuclein.
As part of the study, the scientists included fragments of alpha-synuclein and other proteins that make up neurons in 67 blood samples of patients with Parkinson's disease and 36 blood samples of healthy people of the same age. After that, they analyzed the samples for the development of immune reactions. In the blood samples of people in the control group, there was practically no activation of immune cells, whereas the T-lymphocytes of patients with Parkinson's disease, apparently programmed to recognize alpha-synuclein during earlier interaction with this protein, triggered a strong immune response to fragments of this protein. A particularly pronounced immune response was associated with a genetic variant, the carriers of which are often patients with Parkinson's disease.
The authors suggested that the autoimmune component of Parkinson's disease occurs in cases when neurons lose the ability to get rid of abnormal forms of alpha-synuclein. Young healthy cells effectively break down and remove worn-out and damaged protein molecules, but this ability fades with aging and with certain diseases, including Parkinson's disease. If abnormal alpha-synuclein begins to accumulate in neurons, the immune system unfamiliar with it may mistakenly recognize it as a pathogen and attack.
Currently, researchers are analyzing the immune system's responses to alpha-synuclein on blood samples from additional patients and are working to identify the molecular processes leading to the development of autoimmune reactions in animal and cellular models.
The data obtained can form the basis for the development of tests for the diagnosis of the early stages of Parkinson's disease, as well as the identification of people at risk of developing this disease. The immunotherapeutic approach will increase the tolerance of the immune system of such patients to alpha-synuclein to weaken or prevent the progression of symptoms of the disease.
Article by David Sulzer et al. T cells from patients with Parkinson’s disease recognize alpha-synuclein peptides published in the journal Nature.
Evgeniya Ryabtseva
Portal "Eternal youth" http://vechnayamolodost.ru Based on Columbia University: Parkinson's Is Partly An Autoimmune Disease, Study Finds.
26.06.2017