Does Parkinson’s have an intestinal origin?

PD, or Parkinson’s Disease, was first described in 1817 by the British scientist Dr James Parkinson, and the disease was named after the scientist. Aging is more common, but young people are also affected.

So far, there has been a misconception about Parkinson’s. Evidence from a study in mice suggests that the disease originated in the gut. Most patients with Parkinson’s complain of constipation up to a decade before other symptoms worsen. Parkinson’s is commonly referred to as the tremors, dryness, and difficulty moving that occur as a result of the brain neurons taking over. There are treatments that slow the progression of the disease, but no complete cure has been found.

So far, the whole field of Parkinson’s research has focused on the brain, but now there is evidence to suggest that the disease may have originated in the gut and then spread to the brain.

Researchers often report that patients suffer from constipation and other mood disorders within ten years of the onset of tremors. There is other evidence that the intestinal bacteria in people with Parkinson’s disease are different from those in non-infected adults.

A recent study in mice showed that the toxic fibers formed around the nerve cells of Parkinson’s patients were able to overshadow the nerves of the brain within a few weeks.

“For the first time, I discovered the biological link between intestinal microbiome and Parkinson’s disease,” said Sarkis Mazmanian, lead researcher at the California Institute of Technology (Celtic). “In general, this study reveals the possibility that diseases that cause neurodegeneration in the gut originate, which contradicts the former thinking focused on the brain.”

The team investigated the spread of toxic fibers consisting of substances called alpha-sinusline. Alpha-sinusline is very small and is found in healthy nerve cells. But sometimes, for some unknown reason, these alpha-sinusine molecules stick together to form masses, which eventually turn into the same damaging fibers to the nerves in the brain. About a decade ago, researchers’ papers began to show that fibers in the brains of Parkinson’s patients were also found in their intestines. In a recent study, the Caltech team examined mice that had become genetically vulnerable to Parkinson’s disease by genetically engineering and forcing their bodies to overproduce alpha-sinusline.

Some of these mice were raised in normal, non-sterile cages and others in sterile, germ-free environments. Mice raised in antimicrobial cages showed signs of motor deficiency and less toxic fibers in their brains, but those raised in non-sterile cages showed signs of Parkinson’s as expected.

With antibiotic treatment, the symptoms of non-sterile mice were alleviated; This means that something in their microbiome is exacerbating the symptoms. Finally, the team injected bacteria from human Parkinson’s patients into mass-free mice. After this, the period of decline of these mice intensified sharply. Intestinal bacteria taken from healthy humans had no such effect.

“It was here that we said we found it,” said team member Timothy Sampson. Mice were genetically identical, with the only difference being the presence or absence of gut bacteria. “We were almost certain that gut bacteria played a key and even vital role in regulating Parkinson’s symptoms.”

There is still a long way to go, but if these perceptions are repeated, it will change the therapeutic approach of the medical community. There will be many opportunities to deal with this disease. Of course, any conclusion we draw from mice is not generalizable to humans. Other factors may be involved in human disease. Other studies have suggested that exposure to certain pesticides may be effective.

The team intends to analyze the microbiome obtained from the intestines of patients to find out which microbes play the most important role in making patients vulnerable. In this case, scientists may be able to diagnose the disease before the symptoms appear and the brain is damaged.

Source: Jam Online

Leave a Reply

Your email address will not be published. Required fields are marked *

Back to top button