Many of the studies have reported the molecular changes involved in AD pathology downstream to membrane receptors in the post-synaptic compartment such as protein kinase C (PKC) [124], protein kinase M zeta (PKMζ) [125], calcium/calmodulin-dependent protein kinase II (CaMKII) [126], calcineurin (a phosphatase) [127,128] and cyclic adenosine monophosphate response element binding protein (CREB) [129], all of which affect the maintenance of dendritic spine integrity. This evidence concerns the gene PRRT2 and Alzheimer disease.