However, the mechanisms underlying this effect have not been described in humans, although animal models exposed to cognitive stimulation through exposure to an enriched environment show a decreased production of proinflammatory cytokines such as IL1β, IL-6, and TNF-α through inhibition of NLRP3 inflammasome activation and autophagy [71].Additionally, dysregulation of IL-6 in the bloodstream could contribute to cognitive impairment via synaptic regression and apoptosis of cells, dysregulation of neurotransmitters, demyelination, or neuronal death [71]. The gene discussed is TNF; the disease is Cognitive impairment.