There is no cure for dementia with Lewy bodies (DLB), one of the most common forms of dementia. Previous studies have 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 associated with DLB have not been identified. Now, a group led by researchers at Nagoya University Graduate School of Medicine in Japan has identified three bacteria associated with DLB: Collinsella, Ruminococcus, and Bifidobacterium. Their results, reported in npj Parkinson’s diseasesuggest 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 the transmission of 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 starts with movement problems, but some patients develop cognitive decline within a year. These patients are diagnosed with DLB when this cognitive decline occurs. It is difficult for physicians to predict which people with Parkinson’s disease will experience 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) from Nagoya University Graduate School of Medicine, in collaboration with Okayama Neurology Clinic, Iwate Medical University , and Fukuoka University, analysis of microorganisms in the gut and fecal bile acids of patients with DLB, Parkinson’s disease, and rapid eye movement behavior disorder. They discovered that through intestinal bacteria, Collinsella, Ruminococcus, and Bifidobacterium, which involved patients with DLB. This may suggest possible ways to diagnose and treat this neurodegenerative disease.
The researchers also found similarities between the gut bacteria associated with 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. “Reductions of SCFA-producing bacteria have been repeatedly reported in Parkinson’s disease, Alzheimer’s disease, and ALS,” Ohno explains. “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 the regulation of the immune system by suppressing neuroinflammation.
On the other hand, in patients with DLB, the researchers found an increase in Ruminococcus torqueincrease on Collinsella, and reduction of Bifidobacterium. This was different from Parkinson’s disease patients, whose levels were unchanged. 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 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 related to cognitive decline.
The same, both Ruminococcus torque and Collinsella they are intestinal bacteria that carry an enzyme, the product of which controls inflammation in a region of the brain called the substantia nigra. The substantia nigra produces dopamine, a neurotransmitter involved in the regulation of movement that 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, a key feature that distinguishes DLB from Parkinson’s disease, is delayed.
“Our results can be used for diagnosis and treatment,” explains Ohno. “If a patient with Parkinson’s disease develops dementia within one 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 DLB patient. the gut microbiome to identify such patients.”
“In terms of treatment, the administration of the Ruminococcus torque and Collinsella in patients with Parkinson’s disease to delay neuroinflammation in the substantia nigra,” said Ohno. “Increased therapeutic intervention Bifidobacterium it may delay the onset and progression of DLB and reduce cognitive dysfunction.”
“The presence of intestinal bacteria unique to DLB may explain why some patients develop Parkinson’s disease while others develop DLB first,” Ohno said. “Normalizing the abnormal bacteria shared between DLB and Parkinson’s disease could delay the development of both diseases. Improving the gut microbiota is a step forward in the treatment of dementia. Our findings could pave the way resolve to find new and completely different therapies.”