What question did this study set out to answer?

The study investigates the plasma levels of clusterin, anti-CCP, and anti-GAD antibodies in Parkinson's disease to evaluate their diagnostic and monitoring capabilities.

March 26, 2026Open Access

Monitoring Plasma Indicators in Parkinson’s Disease: A Longitudinal Study of Clusterin, Glutamic Acid Decarboxylase Antibodies, and Anti-Cyclic Citrullinated Peptide Antibodies

Key Points

The study investigates the plasma levels of clusterin, anti-CCP, and anti-GAD antibodies in Parkinson's disease to evaluate their diagnostic and monitoring capabilities.
Analyzed plasma biomarkers in 133 Parkinson's disease patients and 142 healthy controls.
Quantified biomarkers using enzyme-linked immunosorbent assay (ELISA).
Employed Wilcoxon signed ranks and Mann-Whitney U test for statistical comparisons.
Used receiver operating characteristic curve analysis for diagnostic classification.
Plasma levels of clusterin and anti-CCP antibodies were significantly higher in treatment-naive Parkinson's patients compared to healthy controls (p < 0.0001).
Both biomarkers showed significant reductions post-treatment (clusterin: from 126.30 to 115.50 µg/mL; anti-CCP: from 34.80 to 28.70 EU/mL) (p < 0.0001).
Anti-GAD antibody levels did not show significant changes or differences compared to controls (p > 0.05).
ROC analysis indicated significant diagnostic discrimination with area under the curve values of 0.829 for clusterin and 0.713 for anti-CCP, while anti-GAD had an area of 0.509.

Abstract

Objectives The investigation quantified plasma levels of three candidate biomarkers, clusterin (CLU), anti-cyclic citrullinated peptide (anti-CCP) antibodies, and anti-glutamic acid decarboxylase (anti-GAD) antibodies, in a cohort of patients with Parkinson’s disease (PD). The study further assessed longitudinal alterations of these markers in the context of pharmacological intervention, evaluating their discriminatory power against age-matched healthy controls. Material and Methods The study comprised 133 patients with PD and 142 healthy volunteers. Venous blood specimens were procured and processed according to standard immunological protocols, with biomarker quantification performed by enzyme-linked immunosorbent assay (ELISA). Statistically, the Wilcoxon signed ranks and the Mann-Whitney U test were employed for group comparisons, while diagnostic classification was refined by receiver operating characteristic curve analysis. Results Plasma concentrations of CLU and anti-CCP antibodies were markedly elevated in treatment-naive patients with PD relative to healthy controls ( p 0.05). Receiver operating characteristic curve analysis yielded area under the curve values of 0.829 for CLU and 0.713 for anti-CCP, reflecting robust diagnostic discrimination. In contrast, anti-GAD achieved an area of 0.509, indicating a lack of diagnostic capability. Conclusion CLU and anti-CCP antibodies emerge as valuable plasma biomarkers for PD, with their significant post-treatment declines supporting their utility in both diagnosis and monitoring of therapeutic response, in distinction to anti-GAD antibodies, which show no similar link. The adoption of non-invasive plasma-based biomarkers has the potential to refine clinical evaluation and facilitate personalised care in PD. To substantiate these observations and clarify the biomarkers’ relevance to broader clinical practice, further studies with multicentre coordination, large sample sizes, and longitudinal design are imperative.

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