Parkinson’s May Start in the Gut, Not the Brain
New evidence sheds a whole new light on the origins of the disease: have we been wrong about Parkinson’s all along?
Earlier last week, BBC News reported that latest evidence demonstrated close links between Parkinson’s disease (PD), a neurological disorder, and a type of bacteria found in the gut. This finding completely alters the way that we look at the disease, which had previously been thought of as related solely to the brain, and could justify the previously unexplained complaints of constipation and other digestive issues up to a decade before other symptoms arise from sufferers of Parkinson’s.
Parkinson’s disease is a progressive neurological disorder of an unknown cause that leads to loss of dopamine-producing cells in the brain, engendering the decline of brain and motor function. Physical complications such as stiff muscles, involuntary shaking and slow movements, as well as mental health effects like dementia and depression are all typical symptoms of Parkinson’s. The condition is characterised by build-ups Lewy Bodies — aggregates of the protein alpha-synuclein (α-synuclein) — that surround neurones in the substantia nigra, found in the midbrain that is crucial to motor control. It is these neurones in the substantia nigra that are responsible for producing dopamine; thus with sufferers of Parkinson’s, these neurones progressively die and as a result less and less dopamine is produced, causing the symptoms that are seen. It is not clearly understood whether the aggregation of α-synuclein in the substantia nigra is the cause of Parkinson’s disease or a symptom.
The study involved two groups of mice aged 12–13 weeks: one half was genetically engineered to produce α-synuclein while the other half consisted of ‘normal’ mice acting as a control. Within these groups, some mice received gut bacteria taken from human Parkinson’s sufferers, some were given gut bacteria from healthy humans, and others were given nothing at all. The overall results demonstrated a general decrease in the motor functioning of mice with gut bacteria in comparison with the mice that were germ-free. The group of mice that was genetically modified to produce α-synuclein and then given any gut bacteria showed the greatest decline in motor functions, particularly those who were given bacteria from Parkinson’s sufferers who performed the worst in the motor function tests than any other group. Mice producing α-synuclein who remained germ-free still showed motor decline by the time they were 24–25 weeks old; however, the onset of symptoms was significantly slower in comparison to those with any gut bacteria. In addition, antibiotic treatment with those with gut bacteria proved helpful in reducing their symptoms.
So what can we take from these findings? They suggest that the presence of microbiota in the gut regulates and may even play a role in causing the disorder; i.e., what was previously thought of as a condition linked exclusively to the brain has been proven to directly correlate with levels of bacteria in our intestines. This could possibly be a complete game-changer for Parkinson’s — further research could reveal whether the bacteria are the causative agents or simply a piece in the puzzle, and approaches to treatments would be altered radically to effectively slow or even cure the disease. However, it is important not to get too excited too quickly. If one now believes Parkinson’s to be a gut disorder that can be cured with antibiotics, things are, unfortunately, not so easy. We must keep in mind that biological functioning is not identical in mice as it is in humans, and that even once a similar correlation is found in humans, it may still not provide the whole answer as to how Parkinson’s disease is caused. Nevertheless, these findings open gateways for new research that could ultimately revolutionise treatment options provided for Parkinson’s.
