FGF2 and early-onset autosomal dominant Alzheimer disease: 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).