This evidence and some other studies point to a model where an abnormal protein (maybe even a normal one if there were too many of the normal protein) increases in number until it triggers inflammation and some autoimmune process. This could apply to lots of disorders and it could fluctuate over time....
First direct evidence that abnormal protein in Parkinson’s disease triggers immune response.
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, the neurodegenerative movement disorder. The findings raise the possibility that the death of neurons in Parkinson’s could be prevented by therapies that dampen the immune response.
The study, led by scientists at Columbia University Medical Center (CUMC) and the La Jolla Institute for Allergy and Immunology, was published today in Nature.
“The idea that a malfunctioning immune system contributes to Parkinson’s dates back almost 100 years,” said study co-leader David Sulzer, PhD, professor of neurobiology (in psychiatry, neurology and pharmacology) at CUMC. “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.