Figure 3: A putative model illustrating the potential implication of iPLA2γ in Alzheimer’s disease. In this simplified model, iPLA2 dysfunction leads to excessive delivery of GluR1-containing receptors to neuronal membranes. These receptors are more likely to be calcium-permeable and therefore to stimulate calcium influx and, eventually, Tau phosphorylation by calcium-dependent protein kinases such as Cdk5 and GSK-3β.