The first direct evidence that Parkinson's disease is partly an autoimmune disorder in which the tissues are attacked by the body's immune system, found the researchers.
According to the findings, the death of the neurons in Parkinson's could be prevented by therapies that moisten the immune response.
"The idea that a malfunctioning immune system contributes to Parkinson's dates back almost 100 years," said David Sulzer, professor at Columbia University Medical Centre (CUMC) in the US.
"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," said Sulzer.
"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," said Alessandro Sette, professor at La Jolla Institute for Allergy and Immunology.
"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," said Sette.
Scientists were earlier under the belief that neurons were protected from the autoimmune attacks. The new study found that T cells can be tricked intothinking dopamine neurons (those affected by Parkinson'sdisease) are foreign by the buildup of damaged alpha-synucleinproteins, a key feature of Parkinson's disease.
Accoriding to the new study, T cells can be tricked into thinking dopamine neurons (those affected by Parkinson's disease) are foreign by the buildup of damaged alpha-synuclein proteins, a key feature of Parkinson's disease.
"In most cases of Parkinson's, dopamine neurons become filled with structures called Lewy bodies, which are primarily composed of a misfolded form of alpha-synuclein," said Sulzer.
Blood samples from 67 Parkinson's patients and 36 age-matched healthy controls to pieces of alpha-synuclein and other proteins found in neurons were exposed by the researchers.
The samples helped the researchers determine which of the protein fragment caused immune response. In blood samples from the controls, little immune cell activity was seen.
In contrast, T cells in patients' blood samples, whichhad been apparently primed to recognise alpha-synuclein frompast exposure, showed a strong response to the proteinfragments.While T cells in patients' blood samples of patients, which had been apparently primed to recognise alpha-synuclein from past exposure, responded strongly to the protein fragments.
The immune response was associated with a common form of a gene found in the immune system, which may explain why many people with Parkinson's disease carry this gene variant.
Sulzer hypothesises that autoimmunity in Parkinson's disease arises when neurons are no longer able to get rid of abnormal alpha-synuclein.
"If abnormal alpha-synuclein begins to accumulate, and the immune system hasn't seen it before, the protein could be mistaken as a pathogen that needs to be attacked," he said.
Researchers are now analysing these responses in additional patients, and are working to identify the molecular steps that lead to the autoimmune response in animal and cellular models.
"Our findings raise the possibility that an immunotherapy approach could be used to increase the immune system's tolerance for alpha-synuclein, which could help to ameliorate or prevent worsening symptoms in Parkinson's disease patients," said Sette.
(With PTI inputs)