ArticleNPJ Parkinson's disease2023
A proteogenomic view of Parkinson's disease causality and heterogeneity.
Article in NPJ Parkinson's disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Meta-analysis of the make-up and properties of in vitro models of the healthy and diseased blood-brain barrier.Nature biomedical engineering · 2025Pooled it
- Biological heterogeneity in Parkinson's disease: implications for MRI-based patient stratification.NPJ Parkinson's disease · 2026Review
- Sex-aware causal inference assessment of the immune system in complex neurodegenerative diseases.Brain : a journal of neurology · 2026Article
- The complement C3-microglial axis in depression of Parkinson's disease: from mechanism to therapeutic intervention.EBioMedicine · 2026Article
- α-Synuclein-Targeted Immunotherapies in Parkinson's Disease: In Silico, In Vitro and Clinical Perspectives.Molecules (Basel, Switzerland) · 2026Review
- Targeting Mitochondria in Aging-Related Diseases: Therapeutic Potential and Obstacles.MedComm · 2026Review
- Engulfment by brain macrophages in a short-lived vertebrate.bioRxiv : the preprint server for biology · 2026Article
- Plasma proteomics for Parkinson's disease classification: cross-cohort benchmarking of proteomic, transcriptomic, and multimodal models.NPJ Parkinson's disease · 2026Article
- Accelerating Medicines Partnership® Parkinson's Disease Proteomics: A Comprehensive Resource for Advancing Parkinson's Disease Research.Movement disorders : official journal of the Movement Disorder Society · 2026Article
- Identification of circulatory neuro-related proteins in Parkinson's disease: an integrated genetic-proteomic-clinical study.EBioMedicine · 2026Article
- Understanding Neurodegenerative Diseases From the -Omics Perspective: Lessons Learnt.Annals of neurology · 2026Review
- Skeletal Muscle Biomarkers of Amyotrophic Lateral Sclerosis: A Large-Scale, Multi-Cohort Proteomic Study.Annals of neurology · 2026Article
- A neuroimmune-enriched multibiofluid proteomic index associated with cognitive-motor progression in early Parkinson's disease: a longitudinal PPMI cohort study.Frontiers in immunology · 2026Article
- Orthogonal validation of PD Biomarkers: Multi-platform proteomics profiling of CSF, Plasma, and Urine confirms DDC as a consistent candidate.medRxiv : the preprint server for health sciences · 2025Article
- Combining GWAS Summary Data and Proteomics Identified Potential Drug Targets in Dementia.Molecular neurobiology · 2025Article
- Unique nigral and cortical pathways implicated by epigenomic and transcriptional analyses in rotenone Parkinson's model.NPJ Parkinson's disease · 2025Article
- Bidirectional regulation of glycoprotein nonmetastatic melanoma protein B by β-glucocerebrosidase deficiency inbioRxiv : the preprint server for biology · 2025Article
- Multi-omics machine learning classifier and blood transcriptomic signature of Parkinson's disease.Research square · 2025Article
- Beyond oxidative stress: Ferroptosis as a novel orchestrator in neurodegenerative disorders.Frontiers in immunology · 2025Review
- Bibliometric analysis of neural injury biomarkers in neurodegenerative diseases: research trends and future perspectives.Frontiers in human neuroscience · 2025Article
Corrections and comments
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Authors and funding
29 authors at 12 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis and clinical heterogeneity of Parkinson's disease (PD) have been evaluated from molecular, pathophysiological, and clinical perspectives. High-throughput proteomic analysis of cerebrospinal fluid (CSF) opened new opportunities for scrutinizing this heterogeneity. To date, this is the most comprehensive CSF-based proteomics profiling study in PD with 569 patients (350 idiopathic patients, 65 GBA + mutation carriers and 154 LRRK2 + mutation carriers), 534 controls, and 4135 proteins analyzed. Combining CSF aptamer-based proteomics with genetics we determined protein quantitative trait loci (pQTLs). Analyses of pQTLs together with summary statistics from the largest PD genome wide association study (GWAS) identified 68 potential causal proteins by Mendelian randomization. The top causal protein, GPNMB, was previously reported to be upregulated in the substantia nigra of PD patients. We also compared the CSF proteomes of patients and controls. Proteome differences between GBA + patients and unaffected GBA + controls suggest degeneration of dopaminergic neurons, altered dopamine metabolism and increased brain inflammation. In the LRRK2 + subcohort we found dysregulated lysosomal degradation, altered alpha-synuclein processing, and neurotransmission. Proteome differences between idiopathic patients and controls suggest increased neuroinflammation, mitochondrial dysfunction/oxidative stress, altered iron metabolism and potential neuroprotection mediated by vasoactive substances. Finally, we used proteomic data to stratify idiopathic patients into "endotypes". The identified endotypes show differences in cognitive and motor disease progression based on previously reported protein-based risk scores.Our findings not only contribute to the identification of new therapeutic targets but also to shape personalized medicine in CNS neurodegeneration.
Identifiers
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Registered trials
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 Socratic graph.