- Researchers have identified three bacterial strains - Collinsella, Ruminococcus, and Bifidobacterium - linked to Dementia with Lewy bodies (DLB). This discovery could provide potential avenues for the diagnosis and treatment of the neurodegenerative condition.
Dementia with Lewy bodies (DLB), a prevalent form of dementia, currently lacks a cure. Although past research has indicated that gut bacteria may contribute to Parkinson’s disease, the specific bacteria involved in DLB remained unknown. However, scientists at Nagoya University Graduate School of Medicine have recently identified three bacterial strains – Collinsella, Ruminococcus and Bifidobacterium – linked to Dementia with Lewy bodies. Their discovery offers potential new avenues for both diagnosis and treatment of this debilitating condition as reported in npj Parkinson’s Disease.
Abnormal deposits of alpha-synuclein, a protein that facilitates the transmission of signals between neurons in the brain, are linked to the onset of Dementia with Lewy bodies. These deposits, known as Lewy bodies, disrupt chemical processes in the brain and result in cognitive decline affecting memory retention, reasoning ability and thought process. Symptoms may manifest as confusion, impaired movement or visual hallucinations.
Movement problems are typically the first sign of Parkinson’s disease, but some individuals experience cognitive decline within a year and receive a diagnosis of DLB. It is challenging for doctors to anticipate which Parkinson’s patients will develop cognitive impairment and transition into DLB within such a short timeframe.
Associate Professor Masaaki Hirayama from Omics Medicine, Professor Kinji Ohno and Assistant Professor Hiroshi Nishiwaki from Neurogenetics at Nagoya University Graduate School of Medicine, collaborated with Okayama Neurology Clinic, Iwate Medical University, and Fukuoka University to investigate the gut microorganisms and fecal bile acids of patients with DLB, Parkinson’s disease, and rapid eye movement behavior disorder. They found a link between three specific intestinal bacteria – Collinsella, Ruminococcus, and Bifidobacterium – and patients with DLB, which may provide potential avenues for the diagnosis and treatment of this neurodegenerative condition.
The gut bacteria involved in Parkinson’s disease and DLB share similarities, according to the researchers. They discovered that Akkermansia, which breaks down intestinal mucosa, increased in both diseases. Conversely, the gut bacteria responsible for producing short-chain fatty acids (SCFA) decreased. Ohno explains that SCFA-producing bacteria have been consistently found to decrease in neurodegenerative diseases such as Alzheimer’s disease and ALS as well as Parkinson’s disease. This suggests a common feature among these conditions. Regulatory T cells are produced by SCFA, which is crucial because they help regulate the immune system by suppressing neuroinflammation.
In contrast, the study revealed that individuals with DLB exhibited elevated levels of Ruminococcus torques and Collinsella, alongside a reduction in Bifidobacterium. In comparison, Parkinson’s disease patients did not demonstrate any significant changes in their microbiota. These findings may pave the way for doctors to differentiate between DLB and Parkinson’s by examining an individual’s gut bacteria composition in the future.
It is worth noting that the diminished presence of Bifidobacterium could serve as a potential avenue for addressing DLB. This particular strain of bacteria has been shown to boost brain-derived neurotrophic factor, a crucial protein responsible for facilitating the growth and upkeep of neurons in both the central and peripheral nervous systems. As such, its scarcity in individuals with DLB may well contribute to cognitive deterioration.
Likewise, the intestinal bacteria Ruminococcus torques and Collinsella both possess an enzyme that controls inflammation in the substantia nigra region of the brain. This area produces dopamine, a neurotransmitter essential for regulating movement that is often deficient in Parkinson’s disease. In contrast to Parkinson’s disease, individuals with DLB exhibited elevated levels of these bacteria. This disparity may clarify why DLB has a delayed impact on movement, which is a significant distinguishing characteristic between it and Parkinson’s disease.
“Our findings can be used both for both diagnosis and treatment,” explains Ohno. “If a patient with Parkinson’s disease develops dementia in one year after 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 will help to identify such patients.”
Ohno suggested that the introduction of Ruminococcus torques and Collinsella into Parkinson’s patients could delay neuroinflammation in the substantia nigra, which may prove to be an effective treatment option. He further added that therapeutic measures aimed at elevating Bifidobacterium levels could also slow down the onset and advancement of DLB and diminish cognitive impairment.
“The presence of intestinal 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 therapeutics.”