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. 2020 Jul 24;14:762. doi: 10.3389/fnins.2020.00762

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Copyright © 2020 Iannucci, Renehan and Grammas.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Hypothetical scheme for thrombin as a mediator of cerebrovascular activation, neuroinflammation, and neurodegeneration. A hypothetical scheme for thrombin as a mediator of cerebrovascular activation, neuroinflammation, and neurodegeneration. Thrombin can cause neuronal injury directly and indirectly by activation of endothelial cells (ECs) and glia. Thrombin can act on ECs of the blood-brain barrier (BBB) to cause endothelial activation characterized by increased permeability and an increase in reactive oxygen species (ROS), nitric oxide (NO), and inflammatory proteins including thrombin. These toxic vascular-derived products can injure neurons as well as activate neighboring glial cells to release noxious mediators which in turn cause neuronal injury.