ArticleFrontiers in immunology2026
GATD3A-mediated monocyte homeostasis and compartmentalized erythrocyte alpha-synuclein discriminate early Parkinson's disease from MSA-P.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.
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Corrections and comments
- Erratum issued
Authors and funding
11 authors.
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Abstract
Background: Differentiating early-stage Parkinson's disease (PD) from the parkinsonian variant of multiple system atrophy (MSA-P) remains a significant challenge due to overlapping clinical phenotypes. This study aimed to identify novel, minimally invasive biomarkers by integrating high-resolution peripheral monocyte transcriptomics with erythrocytic alpha-synuclein (alpha-Syn) distribution patterns. Methods: We recruited 149 participants (75 PD and 74 MSA-P) to evaluate clinical features and composite peripheral inflammatory indices. To resolve subtle immune heterogeneity often masked in bulk blood analysis, single-cell RNA sequencing (scRNA-seq) was performed on peripheral blood mononuclear cells (PBMCs) from early-stage patients, followed by Quantitative Real-Time PCR (qRT-PCR) validation. Additionally, immunofluorescence was utilized to characterize the subcellular compartmentalization of alpha-Syn forms in erythrocytes. Results: While MSA-P patients exhibited more rapid progression and severe autonomic failure, standard inflammatory markers (e.g., NLR, MLR) failed to distinguish PD from MSA-P in the early clinical stages. However, scRNA-seq revealed distinct monocyte landscapes. Early MSA-P monocytes displayed an aggressive pro-inflammatory profile driven by chemokine upregulation (CXCL10, CXCL5), interferon pathway activation (IFI27). Conversely, early-stage PD monocytes exhibited a profile of precise homeostatic regulation and protective mitochondrial adaptation, characterized by significant GATD3A downregulation verified by qRT-PCR. Furthermore, distinct pathological patterns were identified: oligomeric alpha-Syn was predominantly sequestered on erythrocyte membranes in MSA-P, whereas pS129 alpha-Syn localized primarily to the cytoplasm in PD. Conclusion: This study uncovers a divergent peripheral immune landscape where GATD3A-mediated monocyte homeostasis distinguishes early PD from the chemokine-driven inflammation and intense oxidative stress of MSA-P. Combined with distinct erythrocytic alpha-Syn membrane distribution patterns, these signatures offer a promising multidimensional strategy for the early differential diagnosis of these synucleinopathies.
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