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Year : 2018  |  Volume : 1  |  Issue : 1  |  Page : 20-29

Gut and Parkinson’s disease


1 Director, James Parkinson Movement Disorder Research Centre, Head of Neurology, Kannur Medical College, Kerala, India
2 Junior Resident, Neurology, Kannur Medical College, Kerala, India

Correspondence Address:
Prof. Sujith Ovallath
Director, James Parkinson Movement Disorder Research Centre, Head of Neurology, Kannur Medical College, Kerala
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/AOMD.AOMD_4_18

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Recently it has become increasingly apparent that neurobiological processes can be modified by the bidirectional communication occurring along the brain–gut axis. The microbiota play an important role in this communication through different routes in both physiological and pathological conditions. Gut microbia constitute approximately 100 trillion diverse array of microbes—around 1000 species having greater than 7000 strains—which includes bacteria, yeast, helminthes, protozoa, and viruses. They outnumber human cells and are 150 times the human genes. Most bacteria live in large intestine. There are different causes for the possible gut and Parkinson’s disease (PD) link. Gut is the entry point of many environmental toxins such as pesticides. Pathological deposition of alpha-synuclein starts in the gut several years before the onset of Parkinson symptoms. Constipation is reported as one of the earliest symptoms of PD (4–5 years). Alpha-synuclein is the protein expressed normally in the enteric nervous system (ENS). The level increases by age, but patients with PD have much higher level and early appearance of alpha-synuclein aggregation. Patients with PD show an increased intestinal permeability than the controls due to the defects in intestinal tight junctions. The phenotype is consistent with low-grade intestinal inflammation. Pro-inflammatory immune activity increases the level of alpha-synuclein in gut. Alpha-synuclein can migrate through vagus. It can also enter through circulation into the brain through disrupted blood–brain barrier. Systemic inflammation itself can modify alpha-synuclein in central nervous system. Several strategies are used to prove the gut–brain connection, which could in future be a potential therapeutic option in PD. These include influence of the gut microbiota on brain (viz, germ-free/gnotobiotic animals), use of oral antibiotics (e.g., minocycline, ampicillin to alter gut flora), use of probiotics, and fecal microbiota transplantation.


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