From the perspective of therapeutic considerations, preclinical studies addressing the neuroprotective potential of manipulating certain metabolites associated with various pathways of cerebral ischemia include excitotoxic metabolites using a peptide inhibitor of c-Jun [33], anaerobic glycolysis-induced lactic acidosis using dichloroacetate [34] or induction of normoglycemia [35], and proinflammatory pathway mediators (lysophosphatidylcholines (lysoPCs) and acylcarnitines) using a synthetic agonist for RXR-Nurr1 heterodimer complex [36]. Here, JUN is linked to lactic acidosis.