Scientists have discovered a possible new link between bacterial infections such as tuberculosis and Parkinson’s disease.
Recent research has suggested the protein LRRK2 is involved in the TB disease process. It is also known to be frequently mutated in people with Parkinson’s disease.
Now, Dr Susanne Herbst and colleagues at the Francis Crick Institute, London, UK, show that in cells without LRRK2, Mycobacterium tuberculosis replication is held back.
They believe that the immune mechanism used to clear bacterial infections like tuberculosis may also be implicated in Parkinson’s disease.
The study, published in EMBO Journal yesterday (22 May) might help explain the development of Parkinson’s disease and suggest that drugs designed for Parkinson’s disease – that block LRRK2 – might also be effective for tuberculosis.
Dr Herbst said: "By studying tuberculosis, 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."
Co-author Dr Patrick Lewis added: "Over the last few years, there has been a growing appreciation of the integral role of the immune system in keeping neurons healthy.
"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."
Hartlova, A. et al. LRRK2 is a negative regulator of Mycobacterium tuberculosis phagosome maturation in macrophages. The EMBO Journal 22 May 2018; doi:10.15252/embj.201798694
http://emboj.embopress.org/content/early/2018/05/15/embj.201798694
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