Considering that heightened inflammation and a defective synaptic transmission strongly correlates with the severity of cognitive symptoms in AD (Counts et al., 2014; Selles et al., 2018), we hypothesized that chronic treatment with α-GPC, which sustains Ach release in the hippocampus, could potentially counteract AD-related functional decline. This evidence concerns the gene FGFR3 and Alzheimer disease.