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Monitoring Plasma Indicators in Parkinson’s Disease: A Longitudinal Study of Clusterin, Glutamic Acid Decarboxylase Antibodies, and Anti-Cyclic Citrullinated Peptide Antibodies
*Corresponding author: Prof. Shamsher Singh, Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, India. shamshersinghbajwa@gmail.com
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Received: ,
Accepted: ,
How to cite this article: Rohit, Singh S. Monitoring Plasma Indicators in Parkinson’s Disease: A Longitudinal Study of Clusterin, GAD Antibodies, and Anti-CCP Antibodies. J Health Allied Sci NU. 2026;16:274-81. doi: 10.25259/JHASNU_160_2025
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 <0.0001 for both) and were significantly reduced after 60 days of treatment (CLU: mean change from 126.30 to 115.50 µg/mL; anti-CCP: mean change from 34.80 to 28.70 EU/mL) (p <0.0001 for both), indicating their sensitivity to therapeutic intervention. No post-treatment change in anti-GAD antibody levels was observed, nor was the baseline difference between patients and controls statistically significant (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.
Keywords
Anti-cyclic citrullinated peptide antibody
Clusterin
Glutamic Acid Decarboxylase Antibody
Parkinson’s disease
Plasma biomarkers
INTRODUCTION
Parkinson’s disease (PD) is a neurodegenerative disease marked by tremors, rigidity, and bradykinesia due to degeneration of dopamine-producing neurons in the brain. The precise etiology of PD remains unidentified; nevertheless, it is thought that both hereditary and environmental factors contribute to its development.[1] Contemporary therapies concentrate on the management of symptoms and enhancing the quality of life. The early identification and monitoring of PD are essential for several reasons. Initially, early diagnosis facilitates the swift commencement of therapy, which can aid in symptom management and perhaps decelerate disease development.[2] This line of inquiry has the potential to improve daily functioning and quality of life for those living with PD. In tandem with symptomatic relief, systematic surveillance of disease progression equips clinicians to recalibrate therapeutic regimens in a timely manner. Routine assessment facilitates the appraisal of pharmacological and non-pharmacological interventions, thus guiding evidence-based alterations to care strategies.[3] Accelerated identification together with ongoing surveillance creates the opportunity for expeditious therapeutic and supportive action, with families benefiting from structured education on disease trajectory, lifestyle adaptations, and available resources. Additionally, pro-active management of affective and cognitive sequelae can be instituted, mitigating the cumulative burden of non-motor phenomena. In the present investigation, we quantify the plasma levels of clusterin (CLU), anti-cyclic citrullinated peptide (anti-CCP) antibody, and anti-glutamic acid decarboxylase (anti-GAD) antibodies in a well-characterised cohort of individuals diagnosed with PD. The study further correlates the concentration of each biomarker with established measures of disease severity. By scrutinising these immunological and neurodegenerative signatures, we aspire to delineate their association with disease trajectory and phenotypic expression. Insights gleaned from this investigation may deepen our comprehension of pathophysiological drivers and, ultimately, inform the evolution of diagnostic and therapeutic paradigms in PD.[4] Biomarkers, which provide measurable indicators of pathological states, are proving instrumental for advancing diagnosis, longitudinal assessment, and targeted therapy in PD. Plasma-derived molecules, notably CLU, anti-CCP, and anti-GAD, are gaining attention for their capacity to illuminate disease initiation and progression mechanisms.[5,6] Detectable alterations in their concentrations or multivariate expression profiles within blood-derived plasma may yield critical evidence of neurodegenerative processes and immune dysregulation in individual patients. CLU, also characterised as apolipoprotein J, has long been implicated in neurodegenerative syndromes, including PD. Accumulating data implicates CLU in facilitating alpha-synuclein aggregation, thus contributing to the formation of toxic oligomers that underlie dopaminergic neuron vulnerability within the substantia nigra.[6,7] While anti-CCP antibodies are canonically diagnostic for rheumatoid arthritis, epidemiological observations link their emergence to immune-mediated perturbations in PD; patients exhibit elevated positivity for anti-CCP antibodies relative to neurologically intact controls.[8] Finally, anti-GAD antibodies, which interfere with GABAergic signalling, may further implicate adaptive immune alterations in the disease. Collectively, the converging evidence of these plasma signatures invites further longitudinal studies to establish their utility as diagnostic and prognostic adjuncts in PD. Research into antibodies targeting GAD has extended to autoimmune forms of encephalitis and to specific movement disorder syndromes. Although not well investigated regarding PD, autoimmune processes have been suggested as possible factors in its pathogenesis, with GAD antibodies potentially playing a significant role.[7] The employment of plasma biomarkers in PD research offers several benefits. In contrast to invasive procedures or imaging techniques, collecting plasma samples for biomarker analysis is minimally invasive and economically efficient. The non-invasive characteristic of plasma biomarkers renders them especially appealing for the longitudinal assessment of disease development and therapy efficacy in clinical environments.[9]
MATERIAL AND METHODS
Participants
Study participants were recruited from the neurology department of Guru Gobind Singh Medical College and Hospital in Faridkot. At the same time, the research work (lab test) took place at the ISF College of Pharmacy in Moga, Punjab. We enrolled 133 individuals with PD and 142 individuals who prospectively served as healthy controls [Figure 1]. Patients were eligible if they were at least 18 years old. Those with other neurological and neuromotor disorders, Parkinsonism conditions, or Hemi-PD, in addition to other conditions (infectious, inflammatory, or neoplastic), were not included. Figure 1 shows that all individuals gave their written informed permission before the official screening. Approval from the Institutional Human Ethical Committee with reference number ECR/296/Indt/PB/2022/ISFCP/09 on April 04, 2022, for taking human participants in the study.
- Flowchart illustrating the selection and follow-up process of participants in the study. The flowchart shows two main groups: patients with Parkinson’s disease (PD) and healthy control subjects. For patients with PD, 158 were assessed for eligibility, and 48 were excluded, resulting in 164 included. Out of these, 11 withdrew, 14 were excluded, and 133 completed the study. For healthy controls, 158 were assessed, six declined participation, and 10 were lost to follow-up, resulting in 142 participants who completed the study.
Study criteria
Patients with PD were recruited from the outpatients attending the Clinic for Neurological Disorders, and the control group was recruited from the volunteer participation of individuals. These cases and the control group had different age groups and similar genders. The research was performed according to the Declaration of Helsinki, and all patients signed an informed consent form. The study was carried out by collecting the blood samples and storing them at -70 to -80°C.
Clinical assessment
The diagnosis for PD was made based on the Movement Disorder Society (MDS) Clinical Diagnostic Criteria for PD, which are now considered to be the most reputable criteria in clinical and research fields. Diagnosis was made according to attending to the presence of parkinson’s symptoms (bradykinesia with rest tremor and/or rigidity), lack of absolute exclusion criteria, and fulfilment of supportive criteria such as clear response to dopaminergic therapy. All diagnoses were verified by an experienced neurologist to reach a correct diagnosis.
The severity of PD was defined based on characteristic motor features such as bradykinesia, rigidity, resting tremor, and postural instability during neurological examination by an experienced neurologist.
Sampling techniques
Blood Samples, a total of 5 mL venous blood from each patient and control, were collected as they visited the hospital for their conditions. Blood samples were taken once before starting the medication. Parallel recruitment of PD cases and controls occurred at the same health centres. Blood samples were collected and analysed in the same manner at the ISF College of Pharmacy, Moga, Punjab. Additionally, plasma samples were randomised for examination, with control and PD samples being analysed concurrently on the same microtiter surfaces. Note: Samples were taken carefully in the presence of a physician. The written consent form had been taken from the patient or relatives (if the patient was unable to write).
Assessment of human CLU
The level of CLU in plasma was determined using a commercial kit (Human CLU enzyme-linked immunosorbent assay (ELISA), by Elabscience imported by Labex Corporation). Venous blood samples were taken from all subjects and collected using ethylene-diamine-tetra-acetic acid (EDTA) as an anticoagulant. Plasma samples were centrifuged at 1100 g for 10 min at 4°C, and the supernatant was carefully collected. Each sample, divided into 0.5 mL aliquots, was stored at -70°C until CLU evaluation using a sandwich ELISA method, biotin-labelled antibody. All the procedures were performed as indicated by the manufacturer.
Assessment of anti-GADAs
Serum anti-GAD antibody titers were measured using a commercially available kit [Human anti-GAD ELISA by Elabscience imported by Labex Corporation], which provides a specific and sensitive method for evaluating GAD antibodies. ELISA kits allow quantitative in vitro tests for human auto-antibodies against GAD in serum or EDTA plasma. Within the first step of conducting the ELISA method, the patient’s samples were incubated in wells. If the results were positive, that would indicate a specific binding of antibodies on GAD. Bonded antibodies formed a bridge between GAD in wells and biotin-bonded GAD reagent, which had been added in the next step. In order to detect a bonded biotin, a third incubation was conducted with enzyme-bonded avidin, which catalyses a coloured reaction. The intensity of colouration was proportional to the concentration of antibodies against GAD. All the procedures were performed as indicated by the manufacturer.
Assessment of anti-CCP antibodies
Serum aliquots were stored at -80˚C until the assays were performed. Serum levels of anti-CCP were measured using a commercial ELISA kit (Human anti-CCP ELISA by Elabscience imported by Labex Corporation) according to the manufacturer’s protocol. The cut-off point will be at 20 units/ml.
Statistics
In order to conduct the analysis, the IBM SPSS (Statistical Package for the Social Sciences) Statistics program (version 25; IBM Corp.) was used. For the purpose of ensuring that the findings are interpreted accurately, statistical assumptions were checked for every analysis. It was decided that a p-value of 0.05 would be considered statistically significant. The demographic and clinical data were subjected to statistical analysis, which included the calculation of descriptive statistics such as means, percentages, and standard deviations. Both the first and second assessments were conducted to determine the internal reliability of the domains of each self-report questionnaire. The paired sample and independent sample t-tests were used to investigate the differences in Serum levels of CLU, GAD antibody, and anti-CCP between the case and treatment, case and control, respectively.
RESULTS
Test for normality
Table 1 presents the results of tests of normality for the available biomarkers in different groups. The tests used to assess normality include the Kolmogorov-Smirnov and Shapiro-Wilk tests, which are commonly used to determine whether a data set follows a normal distribution. The table is divided into three main sections: Patient, Treatment, and Control. Under each section, the biomarkers CLU, Glutamic Acid Decarboxylase Antibody, and anti-CCP antibody are examined. For each biomarker, the table provides the statistics for the Kolmogorov-Smirnov and Shapiro-Wilk tests, along with their corresponding degrees of freedom (df) and p values. The p values are used to determine whether the data significantly follow the normal distribution. In the “Control” section, the results for the CLU Level biomarker show a p (>0.05) of 0.200, indicating that the data were not significant and followed a normal distribution. The p values for the other biomarkers suggest significance, which indicates that the data were not normally distributed.
| Groups | Biomarkers | Kolmogorov-Smirnov | Shapiro-Wilk | ||||
|---|---|---|---|---|---|---|---|
| Statistic | df | pvalue | Statistic | df | p value | ||
| Patient | Clusterin level | 0.126 | 121 | 0.0001 | 0.964 | 121 | 0.003 |
| Glutamic acid decarboxylase antibody | 0.165 | 121 | 0.0001 | 0.956 | 121 | 0.001 | |
| Anti-cyclic citrullinated peptide antibody | 0.213 | 121 | 0.0001 | 0.882 | 121 | 0.001 | |
| Treatment | Clusterin level | 0.098 | 121 | 0.006 | 0.963 | 121 | 0.002 |
| Glutamic acid decarboxylase antibody | 0.119 | 121 | 0.0001 | 0.968 | 121 | 0.006 | |
| Anti-cyclic citrullinated peptide antibody | 0.180 | 121 | 0.0001 | 0.887 | 121 | 0.001 | |
| Control | Clusterin level | 0.060 | 121 | 0.200 | 0.971 | 121 | 0.010 |
| Glutamic acid decarboxylase antibody | 0.088 | 121 | 0.022 | 0.967 | 121 | 0.004 | |
| Anti-cyclic citrullinated peptide antibody | 0.148 | 121 | 0.0001 | 0.956 | 121 | 0.001 | |
p >0.05 is significant, df: Degree of freedom.
Patient’s demographic details
A detailed overview of the demographic and medical status characteristics of PD. Table 2 includes the total of 133 patients with PD enrolled in the study, out of which 91 (68.4%) were men and 42 (31.6%) were women, aged range from 54 to 77 years [Median (M) = 64.00, Interquartile Range (IQR) = 6.00] and weight range from 51 to 98 kg (M = 66.00, IQR = 15.50). 142 controls (healthy volunteers), 108 (76.1%) men, and 34 (23.9%) women, age range from 26 to 49 years (M = 38.00, IQR = 8.25), weight range from 46 to 88 kg (M = 71.00, IQR = 14.00). It is evident from the table that there is a slightly higher percentage of male patients in both groups.
| Variable | Patients (n = 133), Frequency (%) | Control (n = 142), Frequency (%) | |||
|---|---|---|---|---|---|
| Gender (Male) | 91 (68.4%) | 108 (76.1%) | |||
| Weight (kg), M (IQR) | 66.00 (15.50), Range: 51-98 | 71.00 (14.00), Range: 46-88 | |||
| Age (Years), M (IQR) | 64.00 (6.00), Range: 54-77 | 38.00 (8.25), Range: 26-49 | |||
| Biomarkers | Without treatment | After 60 days of treatment | |||
| M (IQR) | M (IQR) | Za | M (IQR) | Zb | |
| Clusterin level | 126.3 (4.95) | 115.5 (6.5) | -10.004*** | 61.65 (23.60) | -14.328*** |
| Glutamic acid decarboxylase antibody | 2.6 (1) | 2.6 (0.95) | -1.65 | 2.6 (0.6) | -1.003 |
| Anti-cyclic citrullinated peptide antibody | 34.8 (6.55) | 28.7 (8.3) | -10.008*** | 5.7 (3.1) | -14.33*** |
Patients with Parkinson’s disease without and with treatment, and a control group; a. Performed Wilcoxon Signed Ranks Test (Z), *** p <0.001; b. Performed Mann-Whitney U Test (Z), *** p <0.001. M: Median, IQR: Inter-quartile range.
Plasma concentration of biomarkers
As Table 1 shows, the data were not normally distributed, and the central tendency was measured by M and IQR. The “Biomarkers” section of Table 2 shows the levels of CLU (µg/mL), Glutamic Acid Decarboxylase Antibody (units/mL), and anti-CCP antibody (EU/mL) for patients without treatment and after 60 days of treatment. Additionally, it compares these biomarker levels with the control group. The “Z” represents the results of statistical tests (Wilcoxon Signed Ranks Test and Mann-Whitney U Test) conducted to compare the biomarker levels before and after treatment, as well as between the patient groups and the control group. The p <0.05 denotes the significance of the test results.
Changes in plasma biomarkers
A Wilcoxon signed rank test revealed that CLU and anti-CCP antibody scores were significantly lower after the treatment (treatment group) (M = 115.50, n = 133) and (M = 28.70, n = 133), compared to without treatment (patient group) (M = 126.30, n = 133) and (M = 34.80, n = 133), Z = -10.004 and -10.008, p = 0.0001 and 0.0001, respectively. At the same time, the Glutamic Acid Decarboxylase Antibody score did not show significantly lower values after treatment (M = 2.60, n = 133) compared to those without treatment (M = 2.60, n = 133), Z = -1.650, p = 0.099. Mann-Whitney U Test was performed to identify the significant changes in CLU and anti-CCP antibody of the control group (M = 61.65, n = 142) and (M = 5.7, n = 142), compared to without treatment (patient group) (M = 126.30, n = 133) and (M = 34.80, n = 133), Z = -14.328 and -14.33, p = 0.0001 and 0.0001, respectively. Concurrently, there was no discernible decline in the GAD antibody scores of the control group (M = 2.60, n = 142) compared to the patient group (M = 2.60, n = 133), Z= -1.003, p = 0.316 [Figure 2].
- Clusterin (µg/mL) ● There is a significant difference (p <0.001) between the untreated patients and the control group. Patients show higher levels of CLU, indicating it as a potential diagnostic marker. Post-treatment (60 days): Post-treatment CLU levels in patients significantly decrease (p <0.001), suggesting treatment efficacy. CLU: Clusterin.
- GAD antibody concentration (units/mL) ■ The GAD antibody levels show no significant difference (p >0.05) between untreated patients and the control group. Post-treatment (60 days): There is no significant change in GAD antibody levels after treatment (p >0.05), indicating the limited impact of treatment on this biomarker. GAD: Glutamic acid decarboxylase.
- Anti-CCP antibody concentration (EU/mL) ▲ Anti-CCP antibody levels are significantly different (p <0.001) between untreated patients and controls, indicating potential diagnostic utility. Post-treatment (60 days): Post-treatment levels show a significant decrease (p <0.001), suggesting that treatment effectively reduces anti-CCP antibody levels.
Receiver operating curve (ROC) analysis
Figure 3 illustrates a ROC curve developed to assess the effectiveness of measuring plasma CLU, GAD antibody, and anti-CCP antibody levels in distinguishing between untreated and treated patients. The area under the curve (AUC) serves as an indicator of predictive value, where AUC = 0.5 represents a random association and AUC = 1 signifies perfect discrimination. The AUC values of 0.829 for CLU and 0.713 for anti-CCP antibody indicate that these biomarkers may possess significant diagnostic potential. For the ‘GAD Antibody,’ the area under the receiver operating characteristic curve recorded here is 0.509, thereby demonstrating an absence of sufficient discriminative capacity for diagnostic purposes.
- ROC curve for clusterin; AUC = 0.829. ROC: Receiver operating characteristic, AUC: Area under the curve.
- ROC curve for GAD antibody; AUC = 0.509. ROC: Receiver operating characteristic, GAD: Glutamic acid decarboxylase, AUC: Area under curve.
- ROC curve for anti-CCP antibody; AUC = 0.713. ROC: Receiver operating curve, AUC: Area under the curve.
DISCUSSION
The current paper examined plasma CLU, anti-CCP antibodies, and anti-GAD antibodies, specifically focusing on the changes in these subjects concerning treatment. The data show that CLU and anti-CCP antibodies are higher in untreated PD and decrease during therapy with the dopaminergic activity, indicating that they are correlated with the disease activity and its response. Increasing evidence has linked CLU to neurodegenerative diseases because of its functions in protein homeostasis and neuroinflammation. CLU is proposed to be used as a potential circulating biomarker to detect Parkinson’s in a study by Anjo et al.,[10] which has shown moderate diagnostic accuracy; our findings agree with the findings and further suggest that CLU levels are sensitive to pharmacological intervention, warranting its usage as a monitoring biomarker. Anti-CCP antibodies, which are normally related to autoimmune diseases, have recently been identified as associated with PD. Ebrahimi and Korczyn[11] have displayed higher anti-CCP antibody in patients with PD, especially in patients with dementia; our study enhances this study by depicting the higher anti-CCP antibody in the untreated patients with PD and improvement in the levels after treatment, which suggests the possibility of immune modulation with disease control. On the contrary, the level of anti-GAD antibody was not statistically different between the patients and controls, and remained the same after medication. As previously indicated by Lloyd and Hornykiewicz et al.,[12] Dopaminergic therapy has been shown to change the activity of the glutamic acid decarboxylase enzyme in PD, but our results indicate that the circulating anti-GAD antibodies do not correspond to the changes and thus have limited utility as plasma biomarkers. Analysis of ROC curves also assisted in the diagnostic significance of CLU and anti-CCP antibodies, and anti-GAD antibodies did not demonstrate any significant discriminative power. Taken all, these findings indicate the possible role of the select plasma biomarkers in the evaluation of PD, as well as the importance of additional longitudinal and multicentric research to ensure the clinical utility of these biomarkers.
limitations of the study
Enrolment in the control group was challenging. Many older people have one or more diseases; therefore, it is difficult to find an individual without a disease or disorder.
Future research
The present study was carried out at one research centre; it can be performed at multiple centres in the future. Furthermore, it will be performed on a large sample size of individuals, which will provide precise results as compared to the current study. Chronic treatment may influence the level of GAD in blood plasma. Therefore, long-term research should be conducted.
CONCLUSION
This research examined the levels of CLU, anti-GAD antibodies, and anti-cyclic citrullinated peptide (anti-CCP) antibodies in the plasma of patients with PD and in age-matched healthy controls. Untreated patients had significantly higher CLU and anti-CCP antibody levels than treated patients with PD and controls, and dopaminergic therapy was associated with decreased concentrations of these markers, suggesting that they correlated with the disease state and the response to treatment. Anti-GAD antibody levels, however, were comparable in all groups and hence less relevant as PD biomarkers. Receiver operating characteristic analyses revealed good diagnostic efficiencies of CLU and anti-CCP antibodies, implying their translational value. Taking into account these findings, more extensive and long-lasting studies are necessary to confirm the utility in clinical practice of these biomarkers. In general, CLU and anti-CCP antibodies appear to be hopeful non-invasive biomarkers for PD diagnosis and follow-up. Continued investigation in this area is crucial to enhancing our understanding and management of this complex neurodegenerative disorder.
Ethical approval
The research/study was approved by the Institutional Review Board at ISF College of Pharmacy, Moga, Punjab, number ECR/296/Indt/PB/2022/ISFCP/09, dated 4th April 2022.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patients have given their consent for their clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
Use of artificial intelligence (AI)-assisted technology for manuscript preparation
The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript, and no images were manipulated using AI.
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