Abstract
The use of neuroprosthetic devices has allowed scientists and engineers to study neural populations directly from the central nervous system. These devices are continuously being modified and improved to provide better neural recordings from neural populations of interest due to the significant impact these devices have on assisting individuals who experience paralysis. As a neuroprosthetic device that resides intracortically and therefore subsides intimately with the neural parenchyma, it, however, has a major limitation of creating a local foreign body response. This study exemplifies unique pathways that are activated and disrupted within the central nervous system due to device implantation that can thus decrease the device’s functionality. First and foremost, blood-brain barrier disruption occurs from physical blood vessel disruption from device implantation as well as the molecular degradation of adhesion proteins that bind endothelial cells and make them specialized to the central nervous system. Secondly, a robust activation of NADPH complexes that exacerbate oxidative stress were studied for their known production of reactive oxygen species. Following the study of blood-brain barrier disruption and the activation of NADPH complexes, the complement cascade was revealed to be an active pathway at the device’s interface that exemplifies the foreign body response, nonetheless. The results indicate a vast foreign body response that encompasses each of the pathways that were studied within this project.