Scientists have found that gut bacteria may explain the link between Parkinson’s and IBD.
- People with inflammatory
bowel disease (IBD) have an increased risk of developing Parkinson’s
disease, a neurodegenerative condition.
- Disruption of the gut
microbiome is a feature of both conditions, but experts do not know if
this gut dysbiosis underlies the link between the two diseases.
- A new study comparing the
microbiomes of people with IBD and Parkinson’s disease has found that
people with either condition have depletions in similar types of
beneficial bacteria.
- The findings suggest that
therapies targeting the microbiome to reduce inflammation might reduce
Parkinson’s risk in people with IBD.
Inflammatory
bowel disease (IBD) affects around 5 million
people around the world. It results in a number of gastrointestinal
and other symptoms, which may be alleviated by medications and dietary changes.
Several studies have
suggested that IBD may increase a person’s risk of developing Parkinson’s disease, a neurodegenerative disorder.
One meta-analysis
of studies found that the risk of Parkinson’s was 41% higher in people
with IΒD than in those without the condition.
Gut inflammation is
common in both IBD and Parkinson’s disease. And experts believe that one of the
factors in this gut inflammation is dysbiosis,
or disruption of the gut
microbiome — the huge population of microorganisms that live in the
gastrointestinal (GI) tract.
A new study analyzing
the gut microbiomes of people with IBD and Parkinson’s has found that they
share several differences from the microbiomes of healthy people. Most
noticeably, people with IBD or Parkinson’s had greatly depleted numbers of
bacteria that produce short-chain fatty acids — molecules that modulate the
activity of the immune system.
The research, by
scientists from the University of Florida, is published in npj Parkinson’s disease.
“This is an interesting
study as it is the first time a direct comparison has been made between the gut
microbiome of people with IBD and people with Parkinson’s. It adds to the
emerging picture from previous studies.”— Katherine Fletcher, research
communications Lead, Parkinson’s UK, who was not involved in the study,
The gut microbiome’s
role in IBD and Parkinson’s
Michael
S. Okun, MD, medical advisor at the Parkinson’s Foundation and director at
the Norman Fixel Institute for Neurological Diseases at UF Health, one of the
study authors, told Medical News Today:
“This study identified potential unique features of
the human Parkinson’s and inflammatory bowel disease microbiome and also used
the gut ‘metagenomes’ to shed light on what may be going on in the GI tract.”
To identify whether the
microbiome might help explain epidemiological links between the two diseases,
they recruited 54 people with Parkinson’s disease, 26 with IBD, and 16 healthy
control individuals. All were ages between 40 and 80 years, although those with
Parkinson’s were, on average, older.
All study participants
provided stool samples for analysis. The researchers identified the bacteria
present in these stool samples using metagenomics. For comparison, the researchers also analyzed
large open-access metagenomic datasets from 490 Parkinson’s disease and 234
control samples.
Fewer short-chain
fatty acid-producing bacteria in Parkinson’s, IBD
In people with both Parkinson’s disease and IBD,
several prominent short-chain fatty acid-producing species were depleted. They
also had reduced SCFA synthesis pathways.
“Depletions in
short-chain fatty acid (SCFA)-producing bacteria was one of the most
interesting findings. Additionally, the most striking similarity between
inflammatory bowel disease and Parkinson’s across every dataset was a shared
depletion in similar organisms. One thing that will require a closer look is
the depletions in pathways involved in the synthesis of acetate and butyrate [2
SCFAs] in both Parkinson’s and inflammatory bowel disease. These findings
should raise more dialogue about commonalities in inflammatory pathways.”— Michael
S. Okun, MD
Many of the depleted
bacteria are producers of butyrate, a SCFA that is thought to provide
protection against neurodegeneration. In previous
work, some of the same researchers have shown that people with higher
levels of butyrate in their stool have a later age of onset of Parkinson’s,
suggesting that it may help protect against the disease.
Fletcher highlighted
discovering the depletion of these bacteria may be important:
“SCFA-producing bacteria
release factors that are anti-inflammatory, and gut inflammation is seen in
both IBD and PD and is associated with an increased risk of PD. One of the
factors that SCFA-bacteria produce is butyrate which prevents epigenetic
modification of the genes and this has been associated with neuroprotection in
animal models of PD.”
Gut
dysbiosis may be a cause or consequence
Because this was an
observational study, it cannot determine whether the alterations in the
microbiomes of people with Parkinson’s disease and IBD are causing the disease,
or are a result of the conditions.
The researchers suggest
that inflammation may result in a dysbiotic microbiome, which favours
pathogenic microbes that are able to tolerate more extreme conditions. However,
it is possible that the pathogenic bacteria cause the inflammation.
Possible
treatment options for Parkinson’s and IBD
Previous
research has found that anti-TNF therapies, which are commonly used to
combat inflammation in IBD, may reduce the risk of developing Parkinson’s
disease. However, while their study supported the role of inflammation as a
risk factor, Okun urged caution:
“The data from this study should not become a
rationale for clinicians to reflexively treat already diagnosed or at-risk
folks with anti-TNF therapies. These drugs have risks, and although there may
be future clinical trials, we are not there yet.”
However, Fletcher
highlighted research into the effects of the drugs in people with a similar
condition:
“This hypothesis is
already being tested clinically. People with a sleep disorder called REM sleep
behavior disorder (RBD), who have a very high risk of developing PD within 10
years and also an altered gut microbiome similar to PD, are being tested with
anti-TNF therapy to see whether it slows down or prevents their conversion from
RBD to PD.”
While Okun advised
against the widespread use of pre- and probiotics as their effects may highly
depend on a person’s gut microbiome, Fletcher told us that a healthy diet could
be helpful. She emphasized that the Mediterranean diet, which modifies gut
bacteria in a beneficial way, is associated with a reduced risk of Parkinson’s
disease.
“This work highlights
the importance of being able to pinpoint changes in the gut that might lead to
Parkinson’s and finding ways to intervene. The results also show the importance
of research into diet and supplements for Parkinson’s.”— Katherine Fletcher
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