Journal Article

Peripheral Inflammatory Markers TNF-α and CCL2 Revisited: Association with Parkinson’s Disease Severity

Lampropoulos, Ioannis C., Papoutsopoulou, Stamatia, Xiromerisiou, Georgia, Speletas, Matthaios, Ntavaroukas, Panagiotis, Marogianni, Chrysoula, Androutsopoulou, Anastasia, Kalala, Fani, Dardiotis, Efthimios, Grigoriadis, Nikolaos

2022

Overview

One of the major mediators of neuroinflammation in PD is tumour necrosis factor alpha (TNF-α), which, similar to other cytokines, is produced by activated microglia and astrocytes. Although TNF-α can be neuroprotective in the brain, long-term neuroinflammation and TNF release can be harmful, having a neurotoxic role that leads to death of oligodendrocytes, astrocytes, and neurons and, therefore, is associated with neurodegeneration. Apart from cytokines, a wide family of molecules with homologous structures, namely chemokines, play a key role in neuro-inflammation by drawing cytotoxic T-lymphocytes and activating microglia. The objective of the current study was to examine the levels of the serum TNF-α and CCL2 (Chemokine (C-C motif) ligand 2), also known as MCP-1 (Monocyte Chemoattractant Protein-1), in PD patients compared with healthy controls. We also investigated the associations between the serum levels of these two inflammatory mediators and a number of clinical symptoms, in particular, disease severity and cognition. Such an assessment may point to their prognostic value and provide some treatment hints. PD patients with advanced stage on the Hoehn–Yahr scale showed an increase in TNF-α levels compared with PD patients with stages 1 and 2 (p = 0.01). Additionally, the UPDRS score was significantly associated with TNF-α levels. CCL2 levels, however, showed no significant associations.

• Publisher: MDPI
• Subject: Chemokine CCL2 / Chemokines / Cytokines / Humans / Neuroinflammatory Diseases / Parkinson Disease - diagnosis / Patient Acuity / Tumor Necrosis Factor-alpha