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Parkinson’s Disease Might Originate From Gut Bacteria

The development of Parkinson’s disease might start off from the gut, says a new study published in the journal Cell.

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It is assumed that Parkinson’s disease only involves the brain. After all, the symptoms pertaining to the condition do include tremors and difficulty in moving, problems which are caused by the death of brain neurones. However, a growing body of evidence suggests otherwise, and a more recent study shows that the alimentary canal (more specifically the bacteria it contains) might be involved too.

“We have discovered for the first time a biological link between the gut microbiome and Parkinson’s disease,” says lead author Sarkis Mazmanian, from the Californian Institute of Technology (Caltech).

“More generally, this research reveals that a neurodegenerative disease may have its origins in the gut, and not only in the brain as had been previously thought.”

The new finding is hoped to bring researchers closer to deciphering the cause and understanding the development of the disease, which remain a mystery. It is to be noted that the cure to Parkinson’s has not been found yet. Perhaps, this has been the case because efforts in understanding the cause have only taken into consideration the role of the brain.

Mazmanian and his team set out to study the propagation of toxic fibres that surround the nerve cells of Parkinson’s patients. These threads consist of a molecule called alpha-synuclein. Normally, the latter is soluble and exists as individuals in healthy cells, but the molecules come together into fibres in people affected by the disease, such that brain neurones become damaged. These fibres have also been spotted in the gut of the patients.

The team wanted to evaluate the involvement of these fibres, and they used genetically-modified mice with an over-production of alpha-synuclein fibres; all of these mice were genetically-predisposed to develop the disease. They were kept in different types of environments: normal cages, sterile ones, and non-sterile ones. The results show that the ones from cages with no germs had fewer toxic fibres in their brains while those in non-sterile cages developed the disease; also, the former displayed almost no symptom. Could the bacteria be playing any role? This hypothesis was supported by subsequent findings that showed a reduction in the symptoms of the disease in non-sterile mice when they were given antibiotics. To further test the relevance of the bacteria to the progression of the disease, the team of researchers administered the germ-free mice with gut bacteria taken from humans suffering from the disease: as expected, the mice showed rapid deterioration. On the other hand, when gut bacteria from healthy humans were given to them, no such effect was witnessed.

“This was the ‘eureka’ moment, the mice were genetically identical, the only difference was the presence or absence of gut microbiota,” says co-author Timothy Sampson.

“Now we were quite confident that gut bacteria regulate, and are even required for, the symptoms of Parkinson’s disease.”

More research should be done to confirm the ways in which these gut bacteria might be affecting the brain of Parkinson’s patients. This research suggesting that Parkinson’s originates from the gut might actually clarify certain observations in patients: for instance, the latter will often report digestive problems well before the symptoms of tremors appear. Moreover, other studies appear to back this finding as it has previously been shown that Parkinson’s patients display different gut bacteria as opposed to healthy people.

The next step now is to examine the gut bacteria of the patients.

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