Parkinson’s Disease and gut microbiota
Parkinson's disease is the second most common neurodegenerative disease after
Alzheimer's disease and is hallmarked by damage to the dopaminergic neurons of the substantia nigra of the central nervous system and by alphasynuclein containing inclusion bodies in surviving neurons, resulting in the most noticeable characteristic of the disease: motor impairment.
But the symptoms are not restricted to motor impairment and there are also symptoms such as cognitive impairment, pain, depression, tiredness, orthostatic hypotension and, most commonly, gastrointestinal dysfunction.
In recent years, after the discovery of bidirectional communication between gut and brain, a new focus has been placed on gastrointestinal dysfunctions in Parkinson's disease both in the development and in the exacerbation on symptoms of the disease, influenced by the gut microbiota and mediated by the enteric nervous system (vague nerve).
In this context, the influence of environmental factors on the development and progression of Parkinson's disease via the gut has also been investigated.
Nowadays, non-motor symptoms still remain undertreated, often because of an embarrassment in reporting them or because patients are unaware that these symptoms are related to Parkinson's disease.
Among the most common gastrointestinal symptoms are bloating, drooling, constipation, nausea, delayed gastric emptying and prolonged intestinal transit time. In addition, there are other changes such as increased intestinal permeability associated with presence of alphasynuclein, bacterial translocation, inflammatory processes and oxidative stress and changes in gut microbiota, with reduction of beneficial microorganisms.
It is already known that constipation might precede motor symptoms by over a decade and that the accumulation of alphasynuclein also occurs in the enteric nervous system, associated with damage to enteric neurons and possibly underlie GI dysfunction that reaches the brain via the vagus nerve.
The gut microbiota and its changes, finally, might still play a role in neuronal loss by perpetuating inﬂammatory cascades and oxidative injury in the brain.
Gastrointestinal dysfunctions may also contribute to altered absorption of medication to control motor dysfunctions and improve dopamine neurotransmission, and the consequence is the fluctuation of its metabolic response.
Currently there are not therapeutic strategies that influences the disease progression and none of them directly targets the gut-brain communication. In this sense, Perez-Pardoa et al (2017) did some notes about nutritional intervention with strategies as well as inclusion of membrane precursor phospholipids, prebiotics and probiotics in the improvement of the gastrointestinal symptoms and changes on the composition of the gut microbiota, thus affecting , gut-brain communication.
This post was made mainly for you to know that in 2017 is celebrated the 200th anniversary of the first publication on Parkinson's disease and that despite the many advances much still needs to be understood.
Perez-Pardoa P, Kliesta T, Dodiyab HB, Broersena LM, et al. The gut-brain axis in Parkinson's disease: Possibilities for food-based therapies. European Journal of Pharmacology. 2017.
Abeso JA, Stamelou M, Goetz CG, Poewe W, Lang AE, et al. Past, Present, and Future of Parkinson’s Disease: A Special Essay on the 200th Anniversary of the Shaking Palsy. Movement Disorders. 2017.