Scientists report Parkinson's breakthrough, saying it may help fight TB

Source: Xinhua| 2018-05-22 22:59:25|Editor: yan
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LONDON, May 22 (Xinhua) -- Scientists from a British university and a drugs firm on Tuesday announced that a potential advance in solving the mystery of what caused Parkinson's disease, saying that the finding may also help to combat drug-resistant strains of tuberculosis (TB).

Researchers at the Crick Institute, Newcastle University, and the drugs firm GSK said that they believe that they have uncovered a potential cause of Parkinson's, the degenerative brain disease that affects 145,000 Britons.

The mechanism the human immune cells use to clear bacterial infections like TB might also be implicated in Parkinson's disease, according to the study.

The findings, which will be published in The EMBO Journal, provide a possible explanation of the cause of Parkinson's disease and suggest that drugs designed to treat Parkinson's might also work for TB, which kills 1.67 million people globally every year.

The biological causes of Parkinson's remain largely unknown, making it more difficult to develop and improve treatments.

Discovering a mechanism that causes Parkinson's and how drugs affect it could significantly advance efforts to improve treatments.

These findings in cells were supported by experiments in mice.

When the researchers deleted the gene for LRRK2 in mice, they found that they exhibited an enhanced early immune response to TB infection, and had significantly lower levels of Mtb in their lungs than control mice up to two weeks after infection.

"We think that this mechanism might also be at play in Parkinson's disease, where abnormal masses of protein called 'Lewy bodies' build up in neurons in the brain and cause damage," said Susanne Herbst, joint first author of the paper and post-doctoral fellow at the Crick Institute.

The team suspect that LRRK2 might be preventing immune cells in the brain from degrading cell debris properly, leading to a build-up of protein in neurons that disrupts their function.

"By studying TB, we have found a possible explanation for why LRRK2 mutations are a genetic risk factor for Parkinson's disease," she said. "It's exciting when different fields of research connect up in unexpected ways like this."

Co-author Patrick Lewis, Associate Professor in Cellular and Molecular Neuroscience at the University of Reading, said "The dogma in the Parkinson's field has been to focus almost exclusively on what is happening to neurons in the brain to make them degenerate."

"But over the last few years, there has been a growing appreciation of the integral role of other cells in the brain and particularly the immune system in keeping neurons healthy," Lewis said. "This study reinforces why we should think more broadly about the events that cause neurodegeneration, and that some of the answers to Parkinson's disease might come from immunology."

"Drug-resistant TB is a serious emerging problem, and boosting the body's own immune defense against TB is an important step in the battle against antibiotic resistant strains," said Max Gutierrez, group leader at the Crick and senior author of the paper.

"LRRK2 inhibiting drugs are already being developed to treat Parkinson's disease and we're trying to see if we can repurpose them as a potential new TB therapy," he said.

"This should be relatively straightforward because TB infects the lungs, so the LRRK2 inhibitors wouldn't need to cross the blood-brain barrier like they do in Parkinson's disease," he added.