In the human body, the role of proteins spans across almost every function including providing the building blocks to cells, protecting the body from infection, coordinating chemical reactions and processes in and between cells and transporting important molecules throughout the body. 

DNA in each cell of the body is made up of small regions that provide the instructions for making proteins. These regions are called genes and errors in some of these genes have been associated with an increased risk of developing Parkinson's. Two genes in particular when mutated, PINK1 and PARKIN, are associated with young onset Parkinson's. Exactly why they increase the risk of developing Parkinson's has long been a mystery, but now Canadian scientists have published research that might be able to explain this increased susceptibility.

And it involves the gut and the immune system.

Lab mice are usually kept in very clean environments and are monitored very carefully for infections. But the Canadian researchers purposefully infected young mice that were lacking the PINK1 gene with a bacterium called Citrobacter rodentium. It is very similar to the common human food poisoning bug E. coli. The Citrobacter rodentium caused inflammation in the gut of the mice. Normal mice with a working copy of the PINK1 gene were able to handle this infection, but mice without PINK1 went on to slowly develop Parkinson's-like symptoms.

To investigate why these PINK1 mice started having issues, the researchers investigated the immune system response. They found that while the immune system in normal mice handled the infection in a proper way, the immune cells of the PINK1 mice 'over-reacted'. This resulted in an autoimmune reaction - a state where the immune system starts attacking healthy cells.

Curiously, the Parkinson's-like behaviour features were only a transcient effect, and the PINK1 mice returned to normal 12 months after the infection. The return to normalcy occurred in parallel with the autoimmune reaction easing, and the immune system calming down. This finding points to the potential importance of the immune system in Parkinson's and suggests perhaps that multiple infections may be required for the full blown initiation of Parkinson's. This possibility still needs to be investigated though.

If the findings of this study are independently replicated, they provide compelling evidence for a re-examination of the role of PINK1 (and other genes associated with Parkinson's) in the context of this neurodegenerative condition. It may also point towards novel potential therapeutic opportunities and an important step forward in our understanding of the condition.

Further reading:

Read the full article in Nature News