Orta ve geç evre Parkinson hastalığının CSF'sindeki enflamatuar protein manzarasının ön analizi: motor şiddeti ve alt tipleriyle ilişkiler.

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PurposeParkinson's disease (PD) is a progressive neurodegenerative disorder in which neuroinflammation is recognized as a contributor to clinical progression. This study aimed to characterize the cerebrospinal fluid (CSF) inflammatory profile in mid- to late-stage PD patients and identify specific inflammatory proteins with potential clinical relevance to motor symptoms and disease severity.MethodsIn this preliminary retrospective cross-sectional study, CSF samples were obtained from 25 patients with mid- to late-stage PD undergoing evaluation for deep brain stimulation (DBS) (mean disease duration: 10.24 ± 4.65 years) and 15 non-PD controls (essential tremor or dystonia) undergoing identical surgical procedures. The levels of 92 inflammation-related proteins were quantified using the Olink proximity extension assay (PEA). Based on the identified differentially expressed proteins (DEPs), we next performed preliminary exploratory comparisons of inflammatory profiles between the postural instability and gait difficulty (PIGD, n = 10) and tremor-dominant (TD, n = 10) PD subtypes. Additionally, preliminary correlation analyses were performed between the DEPs and Movement Disorder Society-Unified Parkinson's Disease Rating Scale Part-III (MDS-UPDRS-III) scores to generate preliminary observations with limited clinical inference.ResultsUsing the Olink platform, 28 DEPs were identified between the PD and non-PD groups (p ConclusionIn profiling 92 CSF inflammation-related proteins from 25 advanced PD patients (Hoehn-Yahr 3-4) and 11 controls, we identified 28 upregulated DEPs. IFN-γ emerged as a topologically connected hub in protein-protein interaction networks, and three proteins (IL-10RB, CD8A, CXCL9) showed moderate correlations with motor scores. As cross-sectional descriptive observations, these findings establish a preliminary framework to generate hypotheses for future mechanistic validation and biomarker discovery, while no functional causality can be inferred from the present results.

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