Previously, we have shown that systemic haplodeficiency of either FT or GGT reduces Aβ deposition and neuroinflammation; however, intriguingly, only FT haplodeficiency rescues cognitive deficits in the APP/PS1 transgenic mouse model of AD [27], suggesting distinct roles of FT and GGT in regulating neuronal function. Here, GGT1 is linked to Alzheimer disease.