Somebody was speculating that the frozen shoulder PWP suffer from may not be the inflammation type of frozen shoulder that most people suffer from. An important point as, if not caused by inflammation, then the idea that PD is driven by inflammation and we should all be trying to reduce inflammation might be a red herring.
So I went looking. There is plenty out there on inflammation and PD, but this one stood out:
Parkinson’s Disease: A Systemic Inflammatory Disease Accompanied by Bacterial Inflammagens 2019 ncbi.nlm.nih.gov/labs/pmc/a...
Parkinson’s disease (PD) is a well-known neurodegenerative disease with a strong association established with systemic inflammation. Recently, the role of the gingipain protease group from Porphyromonas gingivalis was implicated in Alzheimer’s disease and here we present evidence, using a fluorescent antibody to detect gingipain R1 (RgpA), of its presence in a PD population. To further elucidate the action of this gingipain, as well as the action of the lipopolysaccharide (LPS) from P. gingivalis, low concentrations of recombinant RgpA and LPS were added to purified fluorescent fibrinogen. We also substantiate previous findings regarding PD by emphasizing the presence of systemic inflammation via multiplex cytokine analysis, and demonstrate hypercoagulation using thromboelastography (TEG), confocal and electron microscopy. Biomarker analysis confirmed significantly increased levels of circulating proinflammatory cytokines. In our PD and control blood analysis, our results show increased hypercoagulation, the presence of amyloid formation in plasma, and profound ultrastructural changes to platelets. Our laboratory analysis of purified fibrinogen with added RgpA, and/or LPS, showed preliminary data with regards to the actions of the protease and the bacterial membrane inflammagen on plasma proteins, to better understand the nature of established PD.
Evidence of systemic inflammation in PD includes the presence of increased levels of circulating cytokines such as IL-1β, IL-2, IL-10, IL-6, IL-4, TNF-α, C-reactive protein, RANTES, and interferon-gamma (INF-γ) (Brodacki et al., 2008; Qin et al., 2016). These markers are accompanied by oxidative stress and might even provide early diagnosis of PD (Lotankar et al., 2017). Recently Rathnayake et al. (2019) evaluated the role of selected serum immune mediators (i.e.,) IFNγ, TNFα, IL10 and NOX in PD progression and estimated their usefulness in preclinical diagnosis. They showed that IFNγ and IL-10 are involved in disease severity and that TNFα-mediated neurotoxicity appears to occur in early PD. In a meta-analysis, aberrations in peripheral cytokine levels were hypothesized to be related to PD, and the authors concluded that higher peripheral concentrations of IL-6, TNFα, IL-1β, IL-2, IL-10, C-reactive protein, and RANTES in patients strengths the clinical evidence that PD is accompanied by an inflammatory response (Qin et al., 2016).
In addition to dysregulated circulating inflammatory molecules, one of the known hallmarks of systemic inflammation is hypercoagulability, or abnormal clotting potential. In PD, changes in the normal clotting of blood have been described (Sato et al., 2003; Rosenbaum et al., 2013; Pretorius et al., 2014, 2018c; Infante et al., 2016; de Waal et al., 2018). Most of these circulating inflammatory biomarkers act as ligands to receptors on platelets (Olumuyiwa-Akeredolu et al., 2019), resulting in downstream signaling events with accompanying platelet hyperactivity and aggregation. RBCs also become eryptotic (programed cell death in RBCs) due to ligand binding and oxidative stress (Pretorius et al., 2014).
Parkin, glutamate, NAC, mitophagy
