Maintenance of Synaptic Stability Requires Calcium-Independent Phospholipase A₂ Activity

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.