A new study published in the journal Nature Communications by the researchers at the La Jolla Institute for Immunology (LJI) explains that Parkinson’s disease is somewhat an autoimmune disease. The specialists report that indications of autoimmunity can show up in Parkinson’s disease patients years before their official diagnosis.
This study is co-led by LJI professor Alessandro Sette, Dr. Biol. Sci and Professor David Sulzer of the Columbia University Medical Center.
Researchers have since a long time ago realized that clusters of a harmed protein called alpha-synuclein develop in the dopamine-producing synapses of patients with Parkinson’s disease. These clusters, in the end, lead to cell death, causing cognitive decline and motor symptoms.
LJI research assistant and Ph.D. professor Cecilia Lindestam Arlehamn tells that when these cells are gone, they can’t come back. If a person can diagnose the disease as right on time as could reasonably be expected, it could have a gigantic effect.
A study in 2017 led by the Sette and Sulzer was the first to show that alpha-synuclein can go about as a reference point for certain T cells and cause them to attack brain cells. This was the primary direct proof that autoimmunity could have a role in Parkinson’s disease.
The recent findings shed light on the reactivity of T cells and disease progression. The blood samples of Parkinson’s disease patients were taken and their T cells were compared with the healthy, age-matched control group. The researchers found that when the patient is first diagnosed with the disease, the T cells that respond to alpha-synuclein are most abundant. These T cells vanish as the disease advances, and some patients still have T cells after 10 years of diagnosis.
The scientists also did an analysis of another patient of Parkinson’s disease whose blood samples were preserved before the disease diagnosis. This analysis helped to understand that T cell response was stronger to alpha-synuclein 10 years before when the patient was not diagnosed with the disease.
Sette tells that identification of T cell response could assist in the analysis of individuals at risk or in the beginning times of disease development, when a large number of symptoms have not been distinguished at this point. Significantly, researchers could dream of a situation where early interference with T cell responses could keep the disease from showing itself or advancing
Sulzer further tells that one of the most significant findings is that the kind of the T cells changes throughout the disease, begins with more aggressive cells and moves to less aggressive cells that may restrain the immune reaction and about ten years later, disappears altogether. The immune responses happen during Parkinson’s disease are almost the same as in the seasonal flue except the changes occur over ten years rather than a week.
Some therapies already exist that are used to treat the disease from autoreactive T cells and these TNF therapies are related to lower frequency of Parkinson’s disease. Going ahead, the analysts are particularly keen on using a device called a T cell-based assay to screen patients who are already at risk for Parkinson’s to check whether TNF treatments could benefit them or not. These patients include individuals with certain genetic mutations and REM sleep disorders.
The scientists hope to study more patients of Parkinson’s disease and tail them over longer timespans to understand better how T cell reactivity changes as the disease advance.