Differences in Blood Metabolite Profiles Identified
"Will Lay the Foundation for Personalized Treatment Development"
A domestic research team has discovered that the presence of REM sleep behavior disorder (RBD), commonly known as sleep talking, significantly affects the pathogenesis of Parkinson's disease.
Hanjoon Kim, Professor of Neurology, Seoul National University Hospital. Seoul National University Hospital
A joint research team consisting of Professors Kim Hanjoon and Jung Kiyeong from Seoul National University Hospital's Department of Neurology, Professor Ko Ara from POSTECH, Professor Lee Seonjae from Gwangju Institute of Science and Technology, and Professor Lee Yeonjong from Sungkyunkwan University School of Medicine announced on August 4 the results of a study in which they classified Parkinson's disease into subgroups based on the presence or absence of RBD and conducted untargeted metabolomic analysis to examine the differences in metabolites in each group.
The research team confirmed that there are differences in blood metabolite profiles between Parkinson's disease patients with RBD and those without RBD. They published significant findings demonstrating that these differences align with the latest theory that classifies Parkinson's disease into "body-first" and "brain-first" types. This suggests that the causes and progression of Parkinson's disease may differ depending on the presence of RBD, and is expected to provide a foundation for the development of more accurate early diagnosis and personalized treatment methods in the future.
Parkinson's disease is a neurodegenerative disorder caused by the gradual destruction of dopamine-producing neurons in the brain. The main symptoms include tremors, muscle rigidity, and slow movements. Non-motor symptoms include constipation, reduced sense of smell, and sleep disorders. Parkinson's disease is a common condition, occurring in about 1% of people over the age of 65 and about 3% of those over 80. In particular, RBD is known as a prodromal symptom of Parkinson's disease, and approximately 5% of RBD patients develop Parkinson's disease each year. However, there are also Parkinson's disease patients without RBD, raising the possibility that the disease pathway or associated factors may differ depending on the presence of RBD.
The research team analyzed plasma samples from a total of 101 participants, including a healthy control group (27 people), an idiopathic RBD group (iRBD, 25 people), a Parkinson's disease with RBD group (PD-RBD+, 25 people), and a Parkinson's disease without RBD group (PD-Only, 24 people). They developed a method using machine learning models to accurately predict the four groups.
The analysis revealed that in the Parkinson's disease with RBD group and the idiopathic RBD group, levels of metabolites derived from gut microbiota, such as p-cresol sulfate, secondary bile acids, and phenylacetylglutamine, were increased. This suggests that Parkinson's disease with RBD is associated with the "body-first" type. In other words, changes in gut microbiota play an important role in the onset of Parkinson's disease, and the disease may progress through interactions between the gut and the brain, as described by the gut-brain axis theory.
In contrast, the Parkinson's disease without RBD group showed increased levels of the stress hormone cortisol and blood glucose, while metabolites such as caffeine, inosine, and uric acid were decreased. This pattern is characteristic of "brain-first" Parkinson's disease.
Professor Kim Hanjoon stated, "Through this study, we have demonstrated that the presence or absence of RBD in Parkinson's disease leads to important differences in pathogenesis and progression. These findings suggest that metabolites derived from gut microbiota could serve as important biological markers for Parkinson's disease, and will provide a crucial foundation for early diagnosis and the development of personalized treatments in the future."
Meanwhile, this study was published in the latest issue of the international journal 'NPJ Parkinson's Disease.'
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