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Tag: parkinsons

Brain Disorder is Closely linked to… the Microbiome?

Parkinson’s disease and the gut microbiome. Two seemingly different topics are actually more related than meets the eye. 

Parkinson’s disease is a neurodegenerative disorder that effects dopamine-producing neurons in the brain. Physical effects of Parkinson’s include tremors, bradykinesia, and limb rigidity. Even though Parkinson’s is the 14th leading cause of death in the United States, the cause and cure remain largely unknown. 

However, a recent study done at the University of Alabama at Birmingham has discovered that there is a link between Parkinson’s disease and the bacteria in the gut microbiome. The gut microbiome contains tens of trillions of microorganisms that are apart of our immune system and metabolism. Approximately one third of the bacteria are common to most people, while the remaining two thirds are specific to oneself and their body. These organisms serve as our own “identity card” that makes us unique. Haydeh Payami, Ph.D., professor in the Department of Neurology in the University of Alabama at Birmingham School of Medicine who lead the study remarked that “the collective genomes of the microorganisms in the gut is more than 100 times larger than the number of genes in the human genome. We know that a well-balanced gut microbiota is critical for maintaining general health, and alterations in the composition of gut microbiota have been linked to a range of disorders.” More specifically, the microbiome helps rid the body of xenobiotics, or chemicals not naturally found in the body often arising from environmental pollutants.

Payami concluded that the research “showed major disruption of the normal microbiome … in individuals with Parkinson’s.” The study followed 197 patients with Parkinson’s from three distinct regions in the United States: New York, Atlanta, and Seattle. Research indicated that patients living in different regions had different gut imbalances, which may reflect the environmental, lifestyle and diet differences between the locations. The study also found that certain medicines used to treat Parkinson’s interact with the gut microbiome differently. It was also noted that the bacteria responsible for removing the aforementioned xenobiotics was different in individuals with Parkinson’s. However, it is still unclear whether Parkinson’s causes changes in an individual’s gut microbiome, or if changes in the microbiome are an early warning sign of the disease. 

The human gut microbiome from this source

Research between the gut microbiome and Parkinson’s is relatively new, so there are no concrete findings or cures yet. Fortunately, this study may hold information for assessing the efficiency or toxicity of medication for the disease by examining its effects in the microbiome. As someone whose relative battled Parkinson’s, I have firsthand witnessed the effects of this terrible disease. It is reassuring to see that there is new research being done every day to eventually find a cure, but in the meantime making the lives of those fighting Parkinson’s easier. As Payami said, “This opens up new horizons, a totally new frontier.”

To read the full study, click here. What do you think: Does Parkinson’s disease change the microbiome or is a change in the microbiome an early indicator of the disease?

Gut Microbes and Parkinson’s Disease: A Fascinating New Study

Parkinson’s, a disease of the central nervous system, affects approximately one million people in the United States. While the disease known for impairing motor skills, it can also have digestive symptoms such as constipation years before diagnosis. Because of this phenomenon, scientists have begun to investigate the role of gut microbiome composition in this awful disease. One such study conducted by a team at Caltech used transgenic mice to get to the answer. All of the mice overexpressed the protein human a-synuclein, which can form the insoluble fibrils that lead to Parkinson’s. However, the researchers raised some of the mice germ-free, or gave them antibiotics, so no intestinal microbes formed. In these mice, Parkinson’s-like symptoms and brain pathology decreased. In addition, the researchers found that the mice that did have gut microbiota had brain inflammation that the germ-free mice didn’t. Only when the researchers fed the germ-free mice short-chain fatty acids (to stimulate gut microbiota) did they show signs of inflammation and other Parkinson’s symptoms. This suggests that gut microbiota that produce short-chain fatty acids could be what triggers this disease.

The researchers then tried to investigate more about which gut bacteria could cause Parkinson’s. Since different communities of gut bacteria live in people with Parkinson’s disease than in healthy people, they wanted to find out if these different communities are merely a byproduct or a cause of the disease. To do so, they transplanted human gut-derived microbes from Parkinson’s patients into some mice, and microbes from healthy people into others. The transgenic mice with microbiota from the Parkinson’s patients ended up with typical Parkinson’s symptoms like motor dysfunction. However, wild-type mice (mice that didn’t overexpress human a-synuclein) weren’t affected. This finding shows that people who are genetically predisposed to Parkinson’s can be afflicted with symptoms if introduced to microbes that are associated with the disease.

This is such groundbreaking work because it establishes a causality between the gut microbiome and Parkinson’s. It also raises questions about the negative affects of short-chain fatty acids on the mice in this study, since they’ve been known to be beneficial in humans. The researchers wish to continue their work by investigating the types of microbes in people with Parkinson’s to get to the fundamental cause of the disease and possible cures.

Do you think that short-chain fatty acids are actually harming humans in unseen ways? Is investigating human gut microbiomes is the right path to find the cure to Parkinson’s? Let me know in the comments!

Three-dimensional Human Intestinal Cells

Human Intestinal Cells Cultured with Gut Bacteria

Credit: Scitechnol Publisher, URL:


Original Article:

Identical Twins, Identical Lives, Different Disease

Jack and Jeff Gernsheimer are identical twins. Jack has Parkinson’s disease, and his twin Jeff does not. Up until recently, because they have identical genomes, it would have been a mystery as to why Jack could develop Parkinson’s but not Jeff. However, with the discovery of epigenetics, scientists know that genes alone cannot explain why some people get Parkinson’s and other do not. While there are some genetic mutations linked to Parkinson’s, 90 percent of cases are “sporadic”, meaning that the disease did not run in the family. Even twins often do not develop Parkinson’s in tandem. Naturally, if genes don’t explain the development of Parkinson’s, scientists look to environment. There are several environmental factors that are known to link to the disease. People who were POW’s in WWII, for example, have a higher rate of developing Parkinson’s. But, and here’s the interesting part, Jack and Jeff have lived almost identical lives. For almost all of their lives, they have lived less than half a mile apart. Throughout their lives, they have been exposed to the same air, water, pesticides, etc. When they grew up, they built homes five minutes apart (by walk) on their father’s farm in Pennsylvania. Then, when they entered the professional life, they co-founded a design firm, working with their desks pushed up against each other.


This anomaly, where a pair of humans exist with the same genetics and the same environment yet only one of them got sick is a research “bonanza” for scientists. All expected variables are being held constant, thus whatever is left must be deeply linked to the origins of Parkinson’s. However, there was a small difference in their lives that could provide insight into this anomaly. in 1968, Jack was drafted into the army and Jeff was not. This led to a series of unfortunate events in Jack’s life: first he served two years stateside in the military, got married, had two children, became involved in a long divorce, and suddenly his teenage son died. After this traumatic event, Jack went on to develop Parkinson’s, glaucoma, and prostate cancer, none of which Jeff has.

Jeff and Jack have been more than willing to undergo several studies in hope of finding something that could alleviate Jack’s Parkinson’s. The first study involved collecting embryonic stem cells from the twins. The benefit of stem cell cultures is that they act similarly to how they would in the body even though they are in a petri dish. The mid-brain dopaminergic neurons grown from Jack’s cells created abnormally low amounts of dopamine. Jeff’s produced normal amounts. Surprisingly, even though Jeff showed no signs of Parkinson’s, both twins had a mutation on a gene called GBA. This gene is known to be associated with Parkinson’s. As a result, both of their brain culture cells produced half the normal amount of beta-glucocerebrosidase, an enzyme linked to that gene. Instead of answering questions, this study only raised more to the fascinating case of Jeff and Jack.

I want to add a bit about how Jack’s son died, because it is unimaginably tragic and can show you just how much Jack had to face. Especially if we are considering Jack’s trauma as a contributor to his development of Parkinson’s, it is important to know the story. When Gabe, Jack’s son, was 14 in 1987, he became fascinated with the Vietnam War. Like any good father, Jack rented his son some movies on the war. One of those being The Deer Hunter, in which there is a scene where two prisoners of the Viet Cong are forced to play Russian Roulette. Gabe told his friend that if it were him, he wouldn’t just sit there. He would rather just get it over with. With that conversation, Gabe got his dad’s pistol, that he knew was hidden in the closet drawer, put one bullet in the chamber, put the gun to his head, and shot.

Jack rarely shows emotion. This “pressure cooker” way of dealing with things could explain his illness. Jeff thinks that the parkinson’s is a physical manifestation of how Jack deals with stress, rather how he doesn’t deal with stress. The connection between stress and disease is a very active research topic. And while their lives were very similar, if compared, Jack’s is by far the life with a more stressful environment. Some research might suggest that this stress differential can have a relation to Parkinson’s disease. In 2002, neuroscientists at UPitt subjected rats to stress, and they found that the stressed rats were more likely to experience damage to their dopamine-producing neurons than the non-stressed rats. This led to the term “neuroendangerment”, which means “rather than stress producing damage directly and immediately, it might increase the vulnerability of dopamine-producing cells to a subsequent insult.”

Another hypothesis as to what caused Jack’s Parkinson’s is that it could be linked to chronic inflammation.  Chronic inflammation is the mechanism by which stress can create neurodegeneration. Evidence that suggests this could be the case in Jack and Jeff is presented in their skin. Jack has psoriasis, a condition linked to chronic inflammation, and Jeff does not.

To this day, the search for what caused Jack’s Parkinson’s continues. Last year, NYSCF scientists conducted a study on the twins’ stem cells. They found a few functional differences between their cells. After finding the GBA mutation, they searched harder for other clues as to what might differentiate their brains. They screened 39,000 SNV’s, single nucleotide variants, which are instances where a single nucleotide in the human genome has been altered (either switched, deleted, or duplicated). They found 11 SNV’s, nine of which are linked to Parkinson’s disease. However, all 9 were found in both twins, meaning that this did not explain why Jack was sick and Jeff wasn’t.

Finally, they were able to uncover a relevant difference. Jack had high levels of MAO-B, which is involved in the breakdown of dopamine, whereas Jeff’s levels were close to normal.This hypothesis supposed that there exists a possible molecular mechanism by which stress could lead to neurodegeneration. What’s nice about this finding is that it could present a possible treatment for Parkinson’s. MAO-B inhibitors exist and are actually drugs currently on the market. They were given to Jack, and while it’s too soon to see the effects and to recommend them as treatment for Parkinson’s disease, it’s definitely a start.


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