Abstract
The available data, including experimental studies, clearly indicate an excessive intravascular activation of circulating platelets in multiple sclerosis (MS) and their hyper-responsiveness to a variety of physiological activators. Platelet activation is manifested as an increased adhesion and aggregation and is accompanied by the formation of pro-thrombotic microparticles. Activated blood platelets also show an expression of specific membrane receptors, synthesis many of biomediators, and generation of reactive oxygen species. Epidemiological studies confirm the high risk of stroke or myocardial infarction in MS that are ischemic incidents, strictly associated with incorrect platelet functions and their over pro-thrombotic activity. Chronic inflammation and high activity of pro-oxidative processes in the course of MS are the main factors identified as the cause of excessive platelet activation. The primary biological function of platelets is to support vascular integrity, but the importance of platelets in inflammatory diseases is also well documented. The pro-thrombotic activity of platelets and their inflammatory properties play a part in the pathophysiology of MS. The analysis of platelet function capability in MS could provide useful information for studying the pathogenesis of this disease. Due to the complexity of pathological processes in MS, medication must be multifaceted and blood platelets can probably be identified as new targets for therapy in the future.
Highlights
Multiple sclerosis (MS) is a major human putative autoimmune, demyelinating, and degenerative disease of the central nervous system (CNS) with a variety of pathophysiological mechanisms, such as axonal injury, neuronal damage, inflammation, demyelination, astrogliosis, and remyelination [1,2].Processes above are not evenly represented in the entire MS population, but can selectively prevail in individual patients
Under the neuroinflammatory conditions caused by the disturbance of blood–brain barrier (BBB), blood platelets quickly adhere to changed endothelium at the sites of vascular injury and became activated
According to research carried out by Laroni et al indicate that treatment of MS patients with disease-modifying drugs (DMDs), especially glatiramer acetate, fingolimod, and dimethyl fumarate significantly enhances the risk of cardiovascular diseases [39]
Summary
Multiple sclerosis (MS) is a major human putative autoimmune, demyelinating, and degenerative disease of the central nervous system (CNS) with a variety of pathophysiological mechanisms, such as axonal injury, neuronal damage, inflammation, demyelination, astrogliosis, and remyelination [1,2]. About 15–20 years after the first symptoms, about three-quarters of cases of RR transform permanently to SP [4] This second form is the more debilitating stage of the disease, characterized by a gradual and irreversible neurological decline. Because activated platelets may adhere to inflamed changed endothelium or proteins present on the subendothelial layer of blood vessel walls, as well as on the tendency to form platelet-leukocyte complexes, allows them to participate in the development of inflammation. Under the neuroinflammatory conditions caused by the disturbance of BBB, blood platelets quickly adhere to changed endothelium at the sites of vascular injury and became activated. Multiple interactions between activated blood platelets and inflammatory cells in the endothelium contribute to neurovascular inflammation. Interactions cell–cell supply crucial mechanisms by which platelets are linking the thrombosis, inflammation, and other related processes [13,14]
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