Higher levels of plasma phosphatidylcholine (17:0_18:1) raise the risk of developing Parkinson’s disease

Abstract Emerging evidence suggests that dysregulation of lipid metabolism and chronic inflammation in the central nervous system (CNS) contribute to the risk of Parkinson’s disease (PD). However, the causal relationship between plasma lipid metabolism and PD, particularly through immune modulation,...

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Main Authors: Daoqing Su, Yajun Jing, Jinye Su, Honglin Zhu, Yiming Chen, Qiu He, Dengliang Wang, Dezhi Kang, Yuanxiang Lin
Format: Article
Language:English
Published: Nature Portfolio 2025-08-01
Series:Scientific Reports
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Online Access:https://doi.org/10.1038/s41598-025-12054-y
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author Daoqing Su
Yajun Jing
Jinye Su
Honglin Zhu
Yiming Chen
Qiu He
Dengliang Wang
Dezhi Kang
Yuanxiang Lin
author_facet Daoqing Su
Yajun Jing
Jinye Su
Honglin Zhu
Yiming Chen
Qiu He
Dengliang Wang
Dezhi Kang
Yuanxiang Lin
author_sort Daoqing Su
collection DOAJ
description Abstract Emerging evidence suggests that dysregulation of lipid metabolism and chronic inflammation in the central nervous system (CNS) contribute to the risk of Parkinson’s disease (PD). However, the causal relationship between plasma lipid metabolism and PD, particularly through immune modulation, remains unclear. In this study, we used Mendelian randomization (MR) to investigate the causal association between plasma lipidome and PD risk, utilizing GWAS summary statistics for PD, circulating immune cells, inflammatory proteins, and plasma lipidome. We found that higher plasma phosphatidylcholine (17:0_18:1) levels were causally associated with an increased risk of PD, with a 1 standard deviation genetically instrumented higher level corresponding to a 30% increased risk (95% CI 1.05–1.61, p = 0.014). Multivariate Mendelian randomization (MVMR) analysis confirmed this association after adjusting for triacylglycerol levels. Mediation analysis revealed that the causal link between plasma phosphatidylcholine and PD was mediated by circulating immune cells (specifically CD45 on CD14+ monocytes and CD45 on HLA-DR+ T cells) rather than by circulating inflammatory proteins. These findings highlight a novel pathway linking lipid metabolism, immune modulation, and PD risk.
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issn 2045-2322
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spelling doaj-art-7f92ee90a7134e7c86353cf1fd601bcc2025-08-20T03:46:04ZengNature PortfolioScientific Reports2045-23222025-08-0115111210.1038/s41598-025-12054-yHigher levels of plasma phosphatidylcholine (17:0_18:1) raise the risk of developing Parkinson’s diseaseDaoqing Su0Yajun Jing1Jinye Su2Honglin Zhu3Yiming Chen4Qiu He5Dengliang Wang6Dezhi Kang7Yuanxiang Lin8Department of Neurosurgery, Neurosurgery Research Institute, The First Affiliated Hospital, Fujian Medical UniversityDepartment of Neurosurgery, Neurosurgery Research Institute, The First Affiliated Hospital, Fujian Medical UniversityDepartment of Neurosurgery, Neurosurgery Research Institute, The First Affiliated Hospital, Fujian Medical UniversityFaculty of Life Sciences and Medicine, King’s College LondonDepartment of Medical Laboratory, College of Medical Technology and Engineering, Fujian Medical UniversityDepartment of Neurosurgery, Neurosurgery Research Institute, The First Affiliated Hospital, Fujian Medical UniversityDepartment of Neurosurgery, Neurosurgery Research Institute, The First Affiliated Hospital, Fujian Medical UniversityDepartment of Neurosurgery, Neurosurgery Research Institute, The First Affiliated Hospital, Fujian Medical UniversityDepartment of Neurosurgery, Neurosurgery Research Institute, The First Affiliated Hospital, Fujian Medical UniversityAbstract Emerging evidence suggests that dysregulation of lipid metabolism and chronic inflammation in the central nervous system (CNS) contribute to the risk of Parkinson’s disease (PD). However, the causal relationship between plasma lipid metabolism and PD, particularly through immune modulation, remains unclear. In this study, we used Mendelian randomization (MR) to investigate the causal association between plasma lipidome and PD risk, utilizing GWAS summary statistics for PD, circulating immune cells, inflammatory proteins, and plasma lipidome. We found that higher plasma phosphatidylcholine (17:0_18:1) levels were causally associated with an increased risk of PD, with a 1 standard deviation genetically instrumented higher level corresponding to a 30% increased risk (95% CI 1.05–1.61, p = 0.014). Multivariate Mendelian randomization (MVMR) analysis confirmed this association after adjusting for triacylglycerol levels. Mediation analysis revealed that the causal link between plasma phosphatidylcholine and PD was mediated by circulating immune cells (specifically CD45 on CD14+ monocytes and CD45 on HLA-DR+ T cells) rather than by circulating inflammatory proteins. These findings highlight a novel pathway linking lipid metabolism, immune modulation, and PD risk.https://doi.org/10.1038/s41598-025-12054-yLipid metabolismParkinson’s diseaseCirculating inflammatory proteinsCirculating immune cellsMendelian randomization analysis
spellingShingle Daoqing Su
Yajun Jing
Jinye Su
Honglin Zhu
Yiming Chen
Qiu He
Dengliang Wang
Dezhi Kang
Yuanxiang Lin
Higher levels of plasma phosphatidylcholine (17:0_18:1) raise the risk of developing Parkinson’s disease
Scientific Reports
Lipid metabolism
Parkinson’s disease
Circulating inflammatory proteins
Circulating immune cells
Mendelian randomization analysis
title Higher levels of plasma phosphatidylcholine (17:0_18:1) raise the risk of developing Parkinson’s disease
title_full Higher levels of plasma phosphatidylcholine (17:0_18:1) raise the risk of developing Parkinson’s disease
title_fullStr Higher levels of plasma phosphatidylcholine (17:0_18:1) raise the risk of developing Parkinson’s disease
title_full_unstemmed Higher levels of plasma phosphatidylcholine (17:0_18:1) raise the risk of developing Parkinson’s disease
title_short Higher levels of plasma phosphatidylcholine (17:0_18:1) raise the risk of developing Parkinson’s disease
title_sort higher levels of plasma phosphatidylcholine 17 0 18 1 raise the risk of developing parkinson s disease
topic Lipid metabolism
Parkinson’s disease
Circulating inflammatory proteins
Circulating immune cells
Mendelian randomization analysis
url https://doi.org/10.1038/s41598-025-12054-y
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