By adopting this model, we have recently demonstrated that both FLX and VTX possess the ability to reverse the depressive-like phenotype and memory deficits induced by the i.c.v. injection of Aβ oligomers in mice, also rescuing the levels of the synaptic proteins synaptophysin and PSD-95 as well as of TGF-β1, the deficit of which has been shown to contribute to inflammation and cognitive decline both in depression and AD (Caraci et al., 2018b; Torrisi et al., 2019). This evidence concerns the gene TGFB1 and Alzheimer disease.