Abstract
Background: Blood levels of immune markers have been proposed to discriminate patients with Parkinson's disease (PD) from controls. However, differences between clinical PD subgroups regarding these markers still need to be identified.Objective: To investigate whether clinical phenotypes can be predicted by the assessment of immune marker profiles in the serum of PD patients.Methods: Phenotypes of clinical PD from Tübingen, Germany (n = 145) and Toronto, Canada (n = 90) were defined regarding clinical subtype, disease onset, severity, and progression as well as presence of cognitive and/or autonomic dysfunction. A panel of serum immune markers was assessed using principal component analysis (PCA) and regression models to define the marker(s) that were associated with clinical phenotypes after adjusting for potential confounders. Findings of both centers were compared for validation. Further, a [18F] FEPPA-PET was performed in a group of patients with high and low values of candidate markers for the assessment of in vivo brain microglial activation.Results: Overall, serum immune markers did not cluster to define a pro/anti-inflammatory profile in PCA. Out of 25 markers only IL-12p40 showed a trend to discriminate between PD subgroups in both cohorts which could not be replicated by [18F] FEPPA-PET.Conclusions: Assessment of cytokines in serum does not reliably differentiate clinical PD subtypes. Accompanying subtype-irrelevant inflammation in PD, dual activity, and lack of specificity of the immune markers, the complex function of microglia, probable effects of treatment, disease stage, and progression on inflammation as well as current technical limitations may limit the usefulness of serum immune markers for the differentiation of subtypes.
Highlights
MATERIALS AND METHODSParkinson’s disease (PD) is one the most frequent movement disorders affecting about 2–3% of the aging population [1]
A total of 145 PD patients from Tübingen and 90 from Toronto were included in the analysis. 14 patients were excluded due to elevated C-reactive protein (CRP)
According to the markers that gather on the same factors, a clear separation between pro- and antiinflammatory marker profiles could not be achieved with principal component analysis (PCA) (Figure 1, Supplementary Table 2)
Summary
MATERIALS AND METHODSParkinson’s disease (PD) is one the most frequent movement disorders affecting about 2–3% of the aging population [1]. It has been estimated that the number of people with PD will double by 2030, indicating a progressive increase in the socio-economic burden in the near future [1] For this reason, understanding the underlying neurodegeneration is vital and the development of disease modifying therapies is urgently needed. It is proposed that this process may lead to nigral cell death Within this context, pro-inflammatory cytokines produced by the microglia are responsible for the activation of the neighboring inactive glial cells and magnify the inflammation. Pro-inflammatory cytokines produced by the microglia are responsible for the activation of the neighboring inactive glial cells and magnify the inflammation In addition they attach to surface cytokine receptors of the dopaminergic cells and trigger apoptosis [3]. Differences between clinical PD subgroups regarding these markers still need to be identified
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