Until now, it was thought among scientists that neurodegenerative diseases such as Parkinson’s lacked autoimmune properties . However, although its origin remains uncertain, its possible relationship with a malfunction of the immune system has long been investigated.
Usually considered a movement disorder, Parkinson’s disease also triggers alterations in cognitive function, in the expression of emotions and in autonomic function . A new study led by David Sulzer, from Columbia University in New York published in Nature , supports this idea and thinks that Parkinson’s, an irreversible and progressive neurodegenerative disease that still has no cure, could be an autoimmune disease. According to Sulzer, two fragments of alpha-synuclein, a protein that accumulates in the brain cells of affected patients, can activate T cells associated with autoimmune attacks. Three years ago, Sulzer had already observed that T cells could mistake neurons damaged by Parkinson’s for external invaders .
In the recent investigation, samples of 67 patients and 36 healthy individuals were compared to observe the differences in their brains. The experts realized that a specific set of molecules derived from alpha-synuclein – which acts as an antigenic determinant manifested by the alleles of the major histocompatibility complex (MHC) – can be recognized by the T cells of patients but not by the of healthy individuals.
One of the functions of MHC proteins is to bind together processed protein fragments and present them on the cell surface where they are analyzed by cells of the immune system. This system ignores most of these fragments, but some of them provoke an inadequate response of T cells. The reaction of these cells depends on a gene involved in the immune system , which would explain the association of the disease with variants of the genes. of MHC that would give rise to an autoimmune response, and that could be the trigger of the disease .
The problem of Parkinson’s worsens at advanced ages and in certain pathologies where the protein recycling process is attenuated and leads to the accumulation of proteins such as alpha-synuclein. If the immune system has not previously detected these proteins, it will mistake them for a pathogen that needs to be confronted and attacked . For now, this team of researchers continues to analyze patient responses to identify the molecular phases that lead to an autoimmune response in animal and cell models. According to Alessandro Sette, study co-author and researcher at the La Jolla Institute for Allergy and Immunology , their discovery raises the possibility that immunotherapy may increase the immune system’s tolerance to alpha-synuclein; This could prevent or prevent Parkinson’s symptoms from getting worse.
References:
Sulzer, D. (2017). T-cells from patients with Parkinson’s disease recognize α-synuclein peptides. Nature. doi:10.1038/nature22815
