Parkinson disease (pd) is a disabling neurodegenerative disease for which there is no cure. Years before the diagnosis of pd patients develop constipation and gastrointestinal intestional issues. Constipation affects over 80% of pd patients.
Recent research shows that the enteric nervous system in the gut and the vagus nerve which anatomically links the gi system to the brain, are severely affected by alpha-synuclein, a protein in lewy bodies. A comprehensive investigation of the relation between human gut microbiome and pd is under way.
Studying the microbiome among individuals who are highly likely to develop pd or are already in the works.
The proposed study will take advantage of 25 years of collected data on environmental and dietary exposures and disease outcomes in two prospective cohorts of men and women.
3. The second brain
Research into the role of the gut microbiome in regulating brain function has increased over the past 10 years. Most of those studies have been done on animal models. Increasing clinical and preclinical evidence implicates the microbiome as a possible key susceptibility factor for neurological disorders, including alzheimer’s disease, autism spectrum disorder, multiple sclerosis, parkinson’s disease, and stroke. Cross-sectional clinical.
The surface of the gut mucosa is the most extensive of the organism and also houses the largest number of lymphoid structures in the human body.
The innervations of the digestive tract are very abundant and are structured in three levels of plexus: functions of the enteric autonomic nervous system include bowel motility, vaso-regulation and permeability control, and secretion of certain gastroenteropancreatic hormones
This multitude of neurons in the enteric nervous system allows us to feel the inner world of our gut and its contents. Much of this neuronal arsenal is evidenced in the elaborate daily routine of digestion, through decomposing food and absorbing nutrients.
Expelling waste requires chemical, mechanical, and rhythmic muscle contractions that move everything to the end. Therefore, equipped with its own reflexes and senses, it can control the behavior of the gut independently of the brain. This nervous system of the intestine is connected to the brain in a bidirectional way.
On one hand, the bowel receives information from the brain, and on the other hand, the bowel sends messages to the brain [ 20 ]. This communication of the intestine with the brain occurs both through the nervous system and the bloodstream and is called the gut-brain axis. Typical examples of this bidirectional circuit would be the increase in intestinal peristalsis (colicky pain and diarrhea) when our brain perceives a danger or, in the opposite direction, the sensation of satiety that our brain perceives when we have ingested a certain quantity of food
The brains of people with parkinson’s disease contain abnormal clumps of proteins called lewy bodies. These clumps are largely made up of the protein alpha-synuclein, which plays a role in crosstalk between brain cells. Lewy bodies interrupt this communication and are thought to be toxic to certain neurons in the brain.
In a major revelation, scientists have discovered that gut bacteria may slow or reverse the development of a protein responsible for parkinson’s disease. According to a daily mail report that cited a university of edinburgh research, study authors identified that bacillus subtilis, a probiotic, stalled the build-up of toxic clumps which deprive the human brain of dopamine. Dopamine allows messages to be transmitted to and from the regions of the brain coordinating the movement of the human body.
A new study adds further evidence to a growing number of research breakthroughs which suggests that parkinson’s (pd) originates in the gut and not the brain. New research outcomes in mice suggest pd might actually start in the gut and this might explain why most parkinson’s patients complain of constipation and gut-related symptoms before other symptoms arise.
Heavy metal toxicity has been reported to be one of the major causes of parkinson’s disease. Dizziness and fainting are some symptoms of low blood pressure, and it is also a result of heavy metal poisoning. The sufferers of parkinson’s disease who are prescribed iron supplements often experience deterioration in their brain health.
2.2. Gut and nervous system
The brain and the gut can interact directly through the vagus nerve, which connects the central nervous system to the heart, lung, and digestive tract. The vagus nerve can be activated by many neuroactive molecules found in the gut. ( 7 ).
Research has associated changes in the gut microbiome with several neurodegenerative and central nervous system diseases, such as alzheimer’s and parkinson’s disease.
For example, it has emerged that patients with alzheimer’s disease have a distinct microbiome composition and decreased microbial diversity compared to healthy individuals. Other recent studies have associated changes in the gut microbiome with multiple sclerosis, amyloid lateral sclerosis and parkinson’s.
fore, the gut microbiome emerges as a potential target for protective measures aiming to prevent pd onset.
3.1. Is the gut autonomous?
Parkinson’s disease (pd) is one of the most common neurodegenerative disorders. Pd patients suffer from gastrointestinal dysfunctions and alterations of the autonomous nervous system
Until now, only little is known about pd-associated changes in gut microbiota composition and their potential implication in pd development. In order to increase knowledge in this field, fecal samples of 34 pd patients and 25 healthy, age-matched control persons were investigated.
Researchers found that the relative abundances of the bacterial genera peptoniphilus, finegoldia, faecalibacterium fusicatenibacter, anaerococcus, bifidobacterium, enterococcus, and ruminococcus were significantly influenced by medication with l-dopa and entacapone, respectively.
New study on development of Parkinson’s disease is ‘on the nose’
With diseases where genetic factors and identified environmental causes account only for a minority of the cases, unidentified environmental factors are believed to play a key role in the initiation and progression of the disease. Such is the case with parkinson’s disease (pd) wherein 90% of cases are of idiopathic nature
The Gut and Parkinson’s Disease: Hype or Hope?
Upon breaking down two decades of research about how the gut affects the brain in parkinson’s disease , a vision for studying the gut-brain connection for the next two decades has been laid out in a review article published in the journal of parkinson’s disease. Specifically, the article, “ the gut and parkinson’s disease: hype or hope? ,” focuses on developing the areas of research for alpha-synuclein pathology, biomarkers, and the gut microbiota and how it relates to the gut-brain connection in the context of parkinson’s disease.
What Do We Know About the Gut Microbiota in Parkinson’s Disease?
We find that gut microbiota is altered in pd and correlate with clinical phenotypes and disease severity in our population. The altered plasma cytokine concentrations associated with specific changes in microbiota further demonstrate that altered microbiome composition alterations with aberrant host immune responses are linked with pd pathogenesis. Elucidating the interplay between microbial and host immune responses will lead to a better understanding of pd pathogenesis.
The emerging role of gut dysbiosis, antibiotics, probiotics, and fecal microbiota transplantation and the role of the microbiome in health and human disease has emerged at the forefront of medicine in the 21st century.
Evidence Suggests Parkinson’s Might Not Start in The Brain
A new study adds to a growing body of research that suggests we might have been thinking about parkinson’s disease wrong this whole time. Instead of being isolated to the brain, new evidence in mice suggests that the condition might actually start in the gut. And it could explain some of the strange coincidences seen in the disease, such as why most parkinson’s patients complain of constipation up to a decade before other symptoms arise.