Various lipids, such as eicosanoids, docosanoids, and cannabinoids, can act as signaling mediators and their abnormal metabolism has implications in AD (Farooqui, 2011) . These lipid mediators can modulate the metabolism of sphingolipids through activation of SMases. Furthermore, sphingolipid-derived molecules such as ceramide and ceramide 1-phosphate can act as lipid mediators and accumulate in the AD brain. This accumulation of sphingolipid derivatives can activate cytosolic phospholipase A 2 (cPLA 2 ), which leads to changes in membrane fluidity and permeability with concomitant alterations in ion homeostasis. Furthermore, the degradation products of cPLA 2 metabolism are often pro-inflammatory (Frisardi et al., 2011) . This work shows how the lipid raft constituents, in this case sphingolipids, can affect AD processes in an APP-independent manner. Here, accumulation and action of these lipid mediators promotes inflammation, a process characteristic of AD (Akiyama et al., 2000) .