Similar signaling platforms operate in neuronal systems, such as that involving estrogen receptor (ER) interactions (reviewed in Marin, 2011) . This signaling mechanism is linked to neurogenesis, neuronal differentiation, synaptic plasticity, and neuroprotection (including against Aβ). Recent research indicates that lipid rafts are the site of formation of a complex between the ER, insulin growth factor 1 receptor (IGF-1R), Cav-1, and a voltage gated anion channel, VDAC. The formation of this signaling complex is neuroprotective but also lipid raft dependent (Marin, 2011) . The "signalosome" paradigm was developed further by Chadwick et al. (2011) who isolated lipid rafts in control and 3xTg AD mice and compared their respective proteomes by mass spectrometry. Proteins so identified were then clustered into specific signaling pathways, which allowed an appraisal of which lipid raft signaling pathways may be altered in AD, rather than changes in individual proteins. This systems biology approach indicated that, in lipid rafts, wild-type mice had higher activation of prosurvival pathways such as PTEN and Wnt/β-catenin, whereas 3xTg mice showed activation of p53 and JNK signaling pathways. In addition, 3xTg mice had a deficit in growth factor signaling, neurodevelopmental signaling and signaling through the sonic hedgehog pathway (Chadwick et al., 2011) . Another proteomic analysis extracted post-synaptic lipid rafts and used LC-MS/MS to analyze their protein content. They found an enrichment of cell adhesion molecules, channels/transporters and G-protein related species. Their data linked lipid rafts to cell adhesion with cell-cell contact regions and cell adhesion points being enriched in rafts. Further to this, H + -ATPase and Na + -K + ATPase are enriched in lipid rafts, being responsible for maintaining ionic gradients and modulating neuronal excitability. This study also found the postsynaptic density to be associated with lipid rafts (Suzuki et al., 2011) . Among channels localized in lipid rafts and involved in maintenance of neuronal cell homeostasis, in particular of astrocytes, are K + -buffering inwardly rectifying Kir4.1 channels and the water channel AQP4 (Hibino and Kurachi, 2007) . Residence in the lipid rafts was also shown to be important for the activity of a member of the chloride channel family, ClC-2, which is widely expressed in the brain and other organs (Cornejo et al., 2009) .