The chronicization of neuroinflammation results in strong changes in the inflammatory profile of microglia, as a consequence of a continuous release of neurotoxic inflammatory mediators, such as inducible nitric oxide synthase (iNOS) and pro-inflammatory cytokines, including IL-1 and tumor necrosis factor TNF-α, clinically resulting in an increased predisposition to the development of cognitive impairment and therefore also associated mood disorders, such as depression [43]. Here, IL1A is linked to depressive disorder.