There might be a link between Tuberculosis (TB) and Parkinson’s according to a study published in The EMBO Journal. This link is related to the mechanism behind how our immune system eradicates bacterial infections. More specifically, the study concluded that the mechanism is the same for Tuberculosis and Parkinson.
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 work for TB too.
For Parkinson's disease, the most common genetic mutation occurs on the LRRK2, which allows the LRRK2 protein overactive. By examining the function of LRRK2 in immune cells known as macrophages that are infected with Mycobacterium tuberculosis (Mtb), the bacterium that leads to TB.
Using a combination of experimental approaches, Crick and GSK researchers, in collaboration with Matthias Trost, a proteomics specialist, from Newcastle University, discovered that LRRK2 inhibits phagosomes from fusing with lysosomes, decreasing their efficacy at clearing bacteria. Deletion of the LRRK2 gene or cell treatment using LRRK2 blockers might significantly reduce the levels of Mtb, treating TB. "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," explains Susanne Herbst, the first author of the study and post-doctoral fellow at the Crick.
Investigators suspect that LRRK2 might inhibit immune cells in the brain from degrading causing a build-up of protein in neurons that disrupts their neuronal function. "By studying TB, we have found a possible explanation for why LRRK2 mutations are a genetic risk factor for Parkinson's disease. It's exciting when different fields of research connect up in unexpected ways like this!" notes Susanne.
The findings also suggest that LRRK2 inhibitors could be a powerful new way for TB treatment. "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. 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."
Sources: Crick