Refine
Has Fulltext
- yes (18)
Is part of the Bibliography
- yes (18)
Year of publication
Document Type
- Journal article (16)
- Report (2)
Language
- English (18)
Keywords
- multiple sclerosis (4)
- Medizin (2)
- NEUROWIND (2)
- blood-brain barrier (2)
- experimental autoimmune encephalomyelitis (2)
- inflammation (2)
- B cells (1)
- C1-inhibitor (1)
- EAE (1)
- FTY720-P (1)
- Glatiramer acetate (1)
- IL-15 (1)
- Inflammation (1)
- K+ channel (1)
- K2P channels (1)
- KCNK5 (1)
- K\(_{2P}\)5.1 (1)
- MIC ligands (1)
- Multiple Sklerose (1)
- NKG2D (1)
- NKG2D ligands (1)
- Neurodegeneration (1)
- Neurologie (1)
- R-715 (1)
- Schlaganfall (1)
- Sphingosine 1-Phosphate (1)
- Stroke (1)
- T cell activation (1)
- T lymphocytes (1)
- TASK2 (1)
- TNF-α (1)
- Wissenschaftlicher Nachwuchs (1)
- Zonula Occludens-1 (1)
- acetylsalicylic acid (1)
- astrocytes (1)
- autoimmune neuroinflammation (1)
- blood coagulation (1)
- celiac disease (1)
- closed head injury (1)
- contact-kinin system (1)
- cutting edge (1)
- dendric cells (1)
- domain potassium channels (1)
- edema (1)
- endothelial cells (1)
- expression (1)
- factor XII (1)
- flu-like symptoms (1)
- glycoprotein VI (1)
- human muscle-cells (1)
- idiopathic inflammatory myopathies (1)
- injection site reactions (1)
- interferon beta (1)
- ion channels (1)
- ischemia (1)
- kinin receptors (1)
- lymphokine-activated killer (1)
- management (1)
- matrix metalloproteinases (1)
- multiple-sclerosis (1)
- neuroinflammation (1)
- novo renal transplantation (1)
- pathology section (1)
- peginterferon bet-1a (1)
- ph (1)
- platelet factor 4 (1)
- platelets (1)
- polymyositis (1)
- potassium channels (1)
- randomized controlled trial (1)
- rat brain microvascular endothelial cell culture (1)
- receptor (1)
- relapsing multiple sclerosis (1)
- thrombosis (1)
- thromboxane (1)
- tight junctions (1)
- traumatic brain injury (1)
- tumor immunity (1)
- up-regulation (1)
- vascular permeability (1)
- volume regulation (1)
- β-APP (1)
Institute
- Neurologische Klinik und Poliklinik (16)
- Neurochirurgische Klinik und Poliklinik (2)
- Rudolf-Virchow-Zentrum (2)
- Deutsches Zentrum für Herzinsuffizienz (DZHI) (1)
- Institut für Anatomie und Zellbiologie (1)
- Institut für Klinische Epidemiologie und Biometrie (1)
- Klinik und Poliklinik für Dermatologie, Venerologie und Allergologie (1)
EU-Project number / Contract (GA) number
- 026155 (1)
Aside from the established immune-mediated etiology of multiple sclerosis (MS), compelling evidence implicates platelets as important players in disease pathogenesis. Specifically, numerous studies have highlighted that activated platelets promote the central nervous system (CNS)-directed adaptive immune response early in the disease course. Platelets, therefore, present a novel opportunity for modulating the neuroinflammatory process that characterizes MS. We hypothesized that the well-known antiplatelet agent acetylsalicylic acid (ASA) could inhibit neuroinflammation by affecting platelets if applied at low-dose and investigated its effect during experimental autoimmune encephalomyelitis (EAE) as a model to study MS. We found that oral administration of low-dose ASA alleviates symptoms of EAE accompanied by reduced inflammatory infiltrates and less extensive demyelination. Remarkably, the percentage of CNS-infiltrated CD4\(^+\) T cells, the major drivers of neuroinflammation, was decreased to 40.98 ± 3.28% in ASA-treated mice compared to 56.11 ± 1.46% in control animals at the disease maximum as revealed by flow cytometry. More interestingly, plasma levels of thromboxane A\(_2\) were decreased, while concentrations of platelet factor 4 and glycoprotein VI were not affected by low-dose ASA treatment. Overall, we demonstrate that low-dose ASA could ameliorate the platelet-dependent neuroinflammatory response in vivo, thus indicating a potential treatment approach for MS.