Principal, with over ten years experience in Research and the Pharmaceutical Industry. Excellent communicator with the ability to manage time efficiently and maintain strong working relationships across teams including external institutions and suppliers. Proven expertise in Pharmacology and Development (R&D), scientific publication, scientific communication & presentation, scientific LeadershipWith more than a decade of work in the area of neuroinflammation pertaining to ischemic damage, it can be stated that neuroinflammation is a complex process. Glutamate and calcium mediated response after ischemic damage has to be addressed immediately (Biomed Pharmacother 2018). Loss of energy levels and mitochondrial damage induced cannot be recovered with antioxidants (Pharmacol Biochem Behav 2011). Among the targets studied, GSK3β could be the best target in comparison to ER or COX. Another observation we propose is that inflammation can be a multiple pathways mediated process arresting of one pathway might stimulate other pathways and mediate the process of inflammation. Though researchers have indicated blocking of inflammatory mechanism at the beginning by prevention of adhesion molecules, arresting leukocyte activity, the expected results have not been obtained. Hence anti-inflammatory drugs alone in the later phase of ischemia cannot prevent neurodegeneration. Based our experience and time dependent alterations in biochemical pathways we propose the following time dependent treatment