In an Alzheimer’s disease model, tcVNS significantly shifted the phenotype of microglial cells from neurodestructive to neuroprotective, increasing the release of BDNF, basic fibroblast growth factor (bFGF), anti-inflammatory cytokines (IL-4, IL-10, TGF-β), and decreasing the release of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), ultimately delaying cognitive decline (162). The gene discussed is FGF2; the disease is Mental deterioration.