In general, lipid rafts can be considered as signaling platforms that bring together various ingredients of the biological membranes determining specificity of the cells and their functioning. They include receptors, channels, recognition molecules, coupling factors and enzymes, facilitating their interaction and supporting signaling. Lipid rafts have been implicated in a plethora of both physiological and pathological processes. Among beneficial processes are axonal growth and branching (Kamiguchi, 2006; Grider et al., 2009; Munderloh et al., 2009 ) and hence raft disruption impedes axonogenesis (Petro and Schengrund, 2009) . Rafts are also involved in the stabilization of synapses (Willmann et al., 2006) . Raft components are also involved in cholera toxin entry via GM1 ganglioside (Holmgren et al., 1973) , HIV-1 entry (gp120), and conversion of prion protein (PrP c ) to its infectious form (PrP Sc ; Fantini et al., 2002; Vieira et al., 2010) . Lipid rafts play a critical role in entry, replication, assembly, and budding of various types of viruses (Suzuki and Suzuki, 2006) . In a more general sense, lipid rafts have been suggested to be involved in cardiovascular disease, carcinogenesis, and immune system diseases (Michel and Bakovic, 2007) . However, this review will focus on the role of lipid rafts in the pathogenesis of AD, a condition with which lipid rafts have been demonstrated to have multifarious links (Cordy et al., 2006; Cheng et al., 2007; Vetrivel and Thinakaran, 2010) .