New York: In what could confirm a century-old suspicion, researchers have found the first direct evidence that autoimmunity — in which the immune system attacks the body’s own tissues — plays a role in Parkinson’s disease, a neurodegenerative disorder.
The finding, published in the journal Nature, raises the possibility that the death of neurons in Parkinson’s could be prevented by therapies that dampen the immune response.
“The idea that a malfunctioning immune system contributes to Parkinson’s dates back almost 100 years,” said study co-leader David Sulzer, Professor at Columbia University Medical Center (CUMC) in the US.
“But until now, no one has been able to connect the dots. Our findings show that two fragments of alpha-synuclein, a protein that accumulates in the brain cells of people with Parkinson’s, can activate the T cells involved in autoimmune attacks,” Sulzer said.
“It remains to be seen whether the immune response to alpha-synuclein is an initial cause of Parkinson’s, or if it contributes to neuronal death and worsening symptoms after the onset of the disease,” study co-leader Alessandro Sette, Professor in the Center for Infectious Disease at La Jolla Institute for Allergy and Immunology in California.
“These findings, however, could provide a much-needed diagnostic test for Parkinson’s disease, and could help us to identify individuals at risk or in the early stages of the disease,” Sette said.
Scientists once thought that neurons were protected from autoimmune attacks. However, in a 2014 study, Sulzer’s lab demonstrated that dopamine neurons (those affected by Parkinson’s disease) are vulnerable because they have proteins on the cell surface that help the immune system recognise foreign substances.
As a result, they concluded, T cells had the potential to mistake neurons damaged by Parkinson’s disease for foreign invaders.
The new study found that T cells can be tricked into thinking dopamine neurons are foreign by the buildup of damaged alpha-synuclein proteins, a key feature of Parkinson’s disease.