ArticleFrontiers in neurology2025
Metabolomic profiling uncovers diagnostic biomarkers and dysregulated pathways in Parkinson's disease.
Article in Frontiers in neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Metabolic Remodeling of the Parkinson's Disease Frontal Cortex Revealed by LC-MS/MS Metabolomics.Biomolecules · 2026Article
- Striatal Metabolomic Profiling Links Brazilian Green Propolis to Suberic Acid Modulation and Nigrostriatal Neuroprotection in a Rat Model of Parkinson's Disease.Molecules (Basel, Switzerland) · 2026Article
- Decoding the Metabolic Signatures of Neurodegeneration Diseases: Advances in Mass Spectrometry-Based Metabolomics.Metabolites · 2026Review
- Nutritional Quality Fingerprinting of Wild and FarmedBiology · 2025Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Parkinson's disease (PD) is the second most common neurodegenerative disorder, and it has an unclear pathogenesis and lacks validated, specific biomarker-based diagnostic approaches, particularly in PD patients with rapid eye movement (REM) sleep behavior disorder (PD-RBD). Methods: Using untargeted liquid chromatography-mass spectrometry (LC-MS) metabolomics, serum profiles of 41 drug-naïve PD patients [including 19 PD-RBD and 22 PD without RBD (PD-nRBD) patients] and 20 healthy controls (HCs) were analyzed. Results: Comparative analyses revealed 144 dysregulated metabolites in PD patients versus HCs, with 7 metabolites-sodium deoxycholate, S-adenosylmethionine, L-tyrosine, 3-methyl-L-tyrosine, 4,5-dihydroorotic acid, (6Z)-octadecenoic acid, and allantoin-demonstrating high classification accuracy [area under the curve (AUC) > 0.93]. Compared with PD-nPBD patients, PD-RBD patients exhibited distinct metabolic profiles, characterized by 21 differentially expressed metabolites, including suberic acid, 3-methyl-L-tyrosine, and methyl (indol-3-yl) acetate (AUC > 0.86). Notably, 3-methyl-L-tyrosine displayed dual dynamics, reflecting dopaminergic depletion in PD and compensatory metabolic adaptations in PD-RBD. Pathway enrichment analysis implicated central carbon metabolism (CCM) disruption in PD and peroxisome proliferator-activated receptor (PPAR) signaling pathway inactivation in PD-RBD. Conclusion: These findings reveal potential serum-based biomarkers for PD and PD-RBD, highlight CCM and PPAR pathways as therapeutic targets, and underscore the role of metabolic dysregulation in PD pathophysiology.
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