Evidence map›Paper›PMID 40750798›Full record

ArticleScientific reports2025

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

Daoqing Su, Yajun Jing, Jinye Su, Honglin Zhu, Yiming Chen, Qiu He, Dengliang Wang, Dezhi Kang, Yuanxiang Lin

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Daoqing Su *Department of Neurosurgery, Neurosurgery Research Institute, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, Fujian, China.
Yajun Jing *Department of Neurosurgery, Neurosurgery Research Institute, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, Fujian, China.
Jinye SuDepartment of Neurosurgery, Neurosurgery Research Institute, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, Fujian, China.
Honglin ZhuFaculty of Life Sciences and Medicine, King's College London, London, UK.
Yiming ChenDepartment of Medical Laboratory, College of Medical Technology and Engineering, Fujian Medical University, Taijiang District, Fuzhou, 350004, Fujian, China.
Qiu HeDepartment of Neurosurgery, Neurosurgery Research Institute, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, Fujian, China.
Dengliang WangDepartment of Neurosurgery, Neurosurgery Research Institute, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, Fujian, China. 827156508@qq.com.
Dezhi KangDepartment of Neurosurgery, Neurosurgery Research Institute, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, Fujian, China. kdz99988@vip.sina.com.
Yuanxiang LinDepartment of Neurosurgery, Neurosurgery Research Institute, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, Fujian, China. lyx99070@163.com.

Funding

National Natural Science Foundation of China 821713273the High level medical and health talents in Jinan City，and 552 Shandong Province Medical and Health Science and Technology Development Program Project 202204040490
6 · The paper itself

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.

Indexed as

Parkinson DiseasePhosphatidylcholinesGenome-Wide Association StudyHumansLipid MetabolismMendelian Randomization AnalysisPolymorphism, Single NucleotideRisk FactorsPhosphatidylcholinesCirculating immune cellsCirculating inflammatory proteinsLipid metabolismMendelian randomization analysisParkinson’s disease

Identifiers

PMID40750798
PMCPMC12317063

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.