You are what you eat

It is a rare day that reading a scientific report of basic research makes the hairs on my neck stand up, but today is one such day. 
An article published in the prestigious journal Neuroncarries the rather dry title “Transneuronal propagation of pathologic α-synuclein from the gut to the brain models Parkinson’s disease”. In their research the authors at Johns Hopkins in Baltimore injected an abnormal protein (α-synuclein preformed fibrils) into the walls of the stomach and intestines of some mice. They left some to develop, but did an operation (that used to be common in humans) to cut the nerve that supplies the stomach in others.

Within one month, the protein was found within the brainstem. At three months this has progressed and the protein is found in the substantia nigra (the ‘seat’ of Parkinson’s) and at seven months this has progressed further in the brain. What’s more, although not seen at 1 or 3 months, by 7 months there was loss of dopamine neurones in the brain and this progressed by 10 months. These changes were not seen in the mice who had the operation.

Not only did they do multiple different kinds of microscopic and imaging experiments to directly detect the spread and progression of this protein, they also looked at the movements and behaviour of the mice. Sure enough, the mice who had the intact nerve (and therefore the spread of the protein to the brain), did worse on movement tests (they were slower and less balanced). They also did significantly worse on memory and decision making tests for mice.
Why is this so (potentially) revolutionary? There are several reasons. 
Firstly, there has been a hypothesis for over 15 years that Parkinson’s starts in the gut and spreads to the brain, and these experiments very strongly support that. This backs up observational data from Scandinavia that showed that humans that had had the nerve-cutting operation (vagotomy) for stomach ulcers were less likely to go on to develop Parkinson’s.
Secondly, not only did these mice show pathological changes on imaging and under the microscope, they behaved like mice with Parkinson’s in many methods of testing. This is all the more novel given that these mice didn’t have any genetic changes that made Parkinson’s more likely – they were ‘ordinary’ mice. Until now animal models of Parkinson’s have been very crude and totally unlike the human form of the pathology (either pure genetic strains or given a toxic compound that causes an ‘instant’ Parkinsons-like picture).
Thirdly, (and leading on from the previous point) with an animal model that is so much more similar to the human form of the disease, it is much more likely that we can identify and try new treatments using this model, that is much more related to human Parkinson’s and therefore much more likely to work for the majority of patients. These treatments need not merely treat the symptoms but genuinely slow, stop or even reverse the condition.
Fourthly (I won’t say finally, because there is so much to unpack from this study), this sheds new light on how Parkinson’s starts, gets to the brain and progresses. The suggestion is that there may be something in the environment that makes its way into individuals and then goes on to cause Parkinson’s. Imagine if we can identify and potentially eliminate that! 
So, for many reasons, this is a truly exciting study, and one that has the potential to revolutionise the field and bring us closer to a cure. One small step for mice, one giant leap for mankind.
The study can be found here.

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