Brooke Derr found this research article via Science Daily, describing an interesting relationship between Parkinson’s Disease and the organism that causes tuberculosis.
Tuberculosis and Parkinson’s disease are both diseases that kill millions of people around the world each year. Parkinson’s disease attacks the nervous system starting with symptoms as little as hand tremors. Eventually the disease progresses to complete stiffness of limbs and possibly death. Although Parkinson’s disease cannot be cured there are medications that can help with the symptoms and even surgery. Tuberculosis attacks the lungs and can be spread through the air. The most common symptom of tuberculosis is coughing. Because the bacteria that causes tuberculosis is very resistant, tuberculosis patients normally have to take several different medications in their treatment. In the article I found, tuberculosis expert and microbiologist, Jeffery Cox has discovered that the protein parkin that causes Parkinson’s disease helps fight tuberculosis. Parkinson’s disease is caused by a fault in the protein called parkin concluding in the impairment of the nervous cells of the body. In the treatment of tuberculosis though, Cox has found that the protein parkin causes elimination of the tuberculosis bacteria. The bacteria Mycobacterium tuberculosis causes tuberculosis. Cox’s research brought him to examine macrophages and mycobacterium.
Macrophages are white blood cells that defend the body from foreign invaders by literally eating them. In its attempt to infect the human body, the Mycobacterium tuberculosis invades the macrophage and the macrophage, in turn, responds by surrounding the bacteria in a sac and moves the sac outside of the cell. Usually the bacteria can escape the sac but then molecules that may escort the bacteria to a lysosome to have it destroyed find it.
The protein parkin is a key player in the autophagy of the mitochondria. Autophagy is the destroying of cellular organelles that are worn out or dysfunctional. The specific term for the destroying of the mitochondria is mitophagy.
When Cox learned that parkin’s alterations or polymorphisms could boost susceptibility to the bacteria it triggered his research. He compared mitophagy and xenophagy (when a cell uses autophagy against a virus or bacteria) of mycobacteria and used the relationship between Parkinson’s polymorphisms and “increased susceptibility to bacterial infection” and came to a reasonable conjecture. He believed that Parkin could be used in xenophagy to kill M. tuberculosis.
In the lab he found that human and mouse macrophages infected with M. tuberculosis utilized parkin to fight the bacteria. Also, it was observed that mice without parkin died after being infected with M. tuberculosis and mice with parkin survived the bacterial infection.
Evolution was the start of the involvement of parkin in organisms older than humans, like flies and mice, long ago to destroy mycobacteria and non-functional or worn out mitochondrion. Cox recognized the Endosymbiont theory to have taken place more than one billion years ago. The Endosymbiont theory is the theory that the mitochondria was a bacteria that was taken up by a eukaryotic cell and instead of being destroyed by that cell, formed a symbiotic relationship with it. Cox has now, after discovering parkin’s potential effects on fighting M. tuberculosis, begun working on amplifying parkin’s action against cell invading bacteria.