Parkinson’s disease also starts with movement problems, but some patients develop cognitive decline within one year. These patients are diagnosed with DLB when this cognitive decline occurs. Physicians find it difficult to predict which people with Parkinson’s disease will develop cognitive decline within a year and become patients with DLB.
A research group led by Associate Professor Masaaki Hirayama (Omics Medicine), Professor Kinji Ohno (Neurogenetics), and Assistant Professor Hiroshi Nishiwaki (Neurogenetics) of Nagoya University Graduate School of Medicine, in collaboration with Okayama Neurology Clinic, Iwate Medical University, and Fukuoka University, analyzed microorganisms in the gut and fecal bile acids of patients with DLB, Parkinson’s disease, and rapid eye movement behavior disorder. They discovered that three intestinal bacteria, Collinsella, Ruminococcus, and Bifidobacterium, were associated with patients with DLB. This may suggest possible ways of diagnosing and treating this neurodegenerative disease.
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The researchers also found similarities between the gut bacteria involved in Parkinson’s disease and DLB. In both diseases, the bacteria Akkermansia, which degrades the intestinal mucosa, increased. On the other hand, the bacteria that produce short-chain fatty acids (SCFA) in the gut decreased. “Decreases in SCFA-producing bacteria have been repeatedly reported in Parkinson’s disease, Alzheimer’s disease, and ALS,” explains Ohno. “This suggests that it is a common feature of neurodegenerative diseases.” SCFA are important because they produce regulatory T cells. These types of cells play a critical role in regulating the immune system by suppressing neuroinflammation.
On the other hand, in patients with DLB, the researchers found an increase in Ruminococcus torques, an increase in Collinsella, and a decrease in Bifidobacterium. This was different from Parkinson’s disease patients, whose levels did not change. In the future using these insights, doctors may be able to analyze the bacteria in a person’s digestive tract to distinguish DLB from Parkinson’s disease.
Importantly, the reduced levels of Bifidobacterium may also suggest possible ways to treat DLB. Bifidobacterium increases brain-derived neurotrophic factor, a key protein that supports the growth, development and maintenance of neurons in the central and peripheral nervous systems. Therefore, its decrease in DLB is likely to be associated with cognitive decline.
Similarly, both Ruminococcus torques and Collinsella are intestinal bacteria that carry an enzyme, the product of which regulates inflammation in a region of the brain called the substantia nigra. The substantia nigra produces dopamine, a neurotransmitter that is involved in the regulation of movement and is deficient in Parkinson’s disease. Compared to Parkinson’s disease, the levels of these bacteria were higher in people with DLB. This may explain why the effect on movement is delayed, a key feature that distinguishes DLB from Parkinson’s disease.
“Our findings can be used both for both diagnosis and treatment,” explains Ohno. “However, we cannot currently predict whether a patient with Parkinson’s disease will become a DLB patient. The gut microbiome will help to identify such patients.”
“In terms of treatment, the administration of Ruminococcus torques and Collinsella in patients with Parkinson’s is expected to delay neuroinflammation in the substantia nigra,” Ohno added. “Therapeutic intervention to increase Bifidobacterium may delay the onset and progression of DLB and reduce cognitive dysfunction.”
“Normalizing the abnormal bacteria shared between DLB and Parkinson’s disease may delay the development of both diseases. Improving the gut microbiota is a stepping stone in the treatment of dementia. Our findings may pave the way for the discovery of new and completely different therapeutics.”
Source: Eurekalert
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