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Background: Parkinson's disease (PD) is a neurodegenerative disorder with a significant immune component, as demonstrated by changes in immune biomarkers in patients' biofluids. However, which specific cells are responsible for those changes is unclear because most immune biomarkers can be produced by various cell types. Objectives: The aim of this study was to explore monocyte involvement in PD. Methods: We investigated the monocyte‐specific biomarker sCD163, the soluble form of the receptor CD163, in cerebrospinal fluid (CSF) and serum in two experiments, and compared it with other biomarkers and clinical data. Potential connections between CD163 and alpha‐synuclein were studied in vitro. Results: CSF‐sCD163 increased in late‐stage PD and correlated with the PD biomarkers alpha‐synuclein, Tau, and phosphorylated Tau, whereas it inversely correlated with the patients' cognitive scores, supporting monocyte involvement in neurodegeneration and cognition in PD. Serum‐sCD163 increased only in female patients, suggesting a sex‐distinctive monocyte response. CSF‐sCD163 also correlated with molecules associated with adaptive and innate immune system activation and with immune cell recruitment to the brain. Serum‐sCD163 correlated with proinflammatory cytokines and acute‐phase proteins, suggesting a relation to chronic systemic inflammation. Our in vitro study showed that alpha‐synuclein activates macrophages and induces shedding of sCD163, which in turn enhances alpha‐synuclein uptake by myeloid cells, potentially participating in its clearance. Conclusions: Our data present sCD163 as a potential cognition‐related biomarker in PD and suggest a role for monocytes in both peripheral and brain immune responses. This may be directly related to alpha‐synuclein's proinflammatory capacity but could also have consequences for alpha‐synuclein processing. © 2020 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society [ABSTRACT FROM AUTHOR]

Background: Remote ischemic conditioning (RIC) is a simple and low-cost intervention that is thought to increase collateral blood flow through the vasodilatory effects of nitric oxide (NO) produced by the endothelium and red blood cells (RBCs). This study aims to investigate whether RIC affects RBC deformability and levels of NO and nitrite in patients with ischemic stroke., Methods: This is a predefined substudy to the RESIST (Remote Ischemic Conditioning in Patients With Acute Stroke Trial) randomized clinical trial conducted in Denmark. RIC was started in the ambulance and continued at the hospital for seven days. Blood samples were collected at different time points: prehospital in the ambulance, in-hospital upon arrival, 2 hours postadmission, and 24 hours postadmission. RBC deformability and erythrocyte aggregation rate were assessed using ektacytometry, NO using flowcytometry, and nitrite content using ozone chemiluminescence., Results: Of 1500 prehospital randomized patients, 486 patients were included in this study between July 28, 2020, and November 11, 2023, and had blood samples taken. Of these, 249 (51%) had AIS, and here RIC treatment was not associated with increased RBC maximal deformability (RIC, 0.549; sham, 0.548; P =0.31), RBC NO (RIC, 35 301 median fluorescence intensity; sham, 34979 median fluorescence intensity; P =0.89), or nitrite (RIC, 0.036 µmol/L; sham, 0.034 µmol/L; P =0.38), but RIC treatment was associated with a significantly reduced aggregation pressure and a slower erythrocyte aggregation rate (RIC, 323.76 millipascal; sham, 352.74 millipascal; P =0.0113)., Conclusions: Prehospital and in-hospital RIC significantly reduced erythrocyte aggregation rate in patients with acute ischemic stroke, while there was no change in RBC deformability, NO content, or whole blood nitrite levels., Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03481777.