Dementia with Lewy bodies (DLB), one of the most common forms of dementia, has no cure. Previous studies suggested that gut bacteria, the microorganisms that live in the human digestive tract, play a role in Parkinson’s disease, another neurodegenerative disorder, but the bacteria involved in DLB had not been identified. Now, a team led by researchers at Nagoya University Graduate School of Medicine in Japan has identified three bacteria involved in DLB: Collinsella, Ruminococcus, and Bifidobacterium. Their findings, reported in npj Parkinson’s diseasethey suggest new ways of diagnosis and treatment.
The onset of DLB is associated with abnormal deposits of alpha-synuclein, a protein in the brain that plays a role in transmitting signals between neurons. The presence of these deposits, known as “Lewy bodies”, affects chemicals in the brain, leading to a decline in thinking, reasoning and memory. Symptoms include confusion, memory loss, impaired movement and visual hallucinations.
Parkinson’s disease also begins with movement problems, but some patients develop cognitive decline within a year. These patients are diagnosed with DLB when this cognitive decline occurs. Doctors have difficulty predicting which people with Parkinson’s disease will experience cognitive decline within a year and become DLB patients.
A research team led by Associate Professor Masaaki Hirayama (Omics Medicine), Professor Kinji Ohno (Neurogenetics) and Assistant Professor Hiroshi Nishiwaki (Neurogenetics) of Nagoya University School of Medicine, in collaboration with Okayama Neurology Clinic, Fukuoka Medical University, analyzed microorganisms in the gut and stool bile acids of patients with DLB, Parkinson’s disease and rapid eye movement disorder. They discovered that three gut bacteria, Collinsella, Ruminococcus, and Bifidobacterium, were associated with DLB patients. This may suggest possible ways to diagnose and treat this neurodegenerative disease.
The researchers also found similarities between the gut bacteria involved in Parkinson’s disease and DLB. In both diseases, bacteria Ackermansia, which degrades the intestinal mucosa, increased. On the other hand, short-chain fatty acid (SCFA)-producing bacteria 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.” SCFAs are important because they produce regulatory T cells. These cell types 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 torquesincrease in Collinsella, and decrease in Bifidobacterium. This was different from patients with Parkinson’s disease, whose levels did not change. In the future, using these ideas, doctors may be able to analyze the bacteria in a person’s digestive tract to distinguish DLB from Parkinson’s disease.
Its reduced levels are significant Bifidobacterium it can 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 system. Therefore, its reduction in DLB is likely to be associated with cognitive decline.
Likewise both Ruminococcus torques and Collinsella are intestinal bacteria that carry an enzyme whose product regulates inflammation in an area of the brain called the substantia nigra. The substantia nigra produces dopamine, a neurotransmitter involved in regulating movement that is deficient in Parkinson’s disease. Compared to Parkinson’s disease, 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 for both diagnosis and treatment,” explains Ohno. “If a patient with Parkinson’s disease develops dementia within a year of the onset of motor symptoms, they are diagnosed with DLB. However, we cannot currently predict whether a patient with Parkinson’s disease will become a patient with DLB. The gut microbiome will help identify such patients.”
“In terms of treatment, the administration of it Ruminococcus torques and Collinsella in Parkinson’s patients is expected to delay neuroinflammation in the substantia nigra,” Ohno added. “Therapeutic intervention will increase Bifidobacterium may delay the onset and progression of DLB and reduce cognitive impairment.”
“The presence of gut bacteria unique to DLB may explain why some patients develop Parkinson’s disease and others develop DLB first,” Ohno said. “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 therapeutic methods.”
(tags For Translation) Parkinson