Finally, inhibiting the active form of GSK-3β is useful for the induction of LTP.34 Presenilin 1(PS1), a product of the PSEN1 gene, is an important causative factor for familial Alzheimer’s Disease (FAD), and also plays a key role in cleaving APP.35 GSK-3β-mediated PS1 phosphorylation affects its interaction with N-cadherin and disrupts their binding interaction, finally leading to neuronal activity deficits and synaptic functioning deficits.36 The interplay among GSK-3β, PS1, and its impact on synaptic functioning deficits and Aβ metabolism can contribute to the pathogenesis of AD. This evidence concerns the gene CDH2 and familial Alzheimer disease.