Ever since the initial descriptions and characterizations of lipid rafts, the field has been beset by controversy (Pike, 2009 ) from their very existence down to the very specific aspects of how to isolate these structures in the laboratory. However, current consensus is that lipid rafts do represent dynamic structural components of cellular membranes integrating signaling events and regulating cell functioning and that their dysregulation can lead to disease. This review has largely concentrated on the links between lipid rafts and AD pathology since processing of AD-related APP and production of Aβ peptide are clearly affected by lipid rafts. Also Aβ signaling involves interactions of proteins resident to lipid rafts. The mechanism underlying these effects has been examined in some detail although numerous gaps in knowledge still remain. Although the attempts to modulate lipid rafts and hence amyloidogenic processing have failed to translate into successful drugs, some epidemiological studies still indicate that inhibition of cholesterol synthesis through statin treatment might be beneficial if applied early (Solomon and Kivipelto, 2009; Shepardson et al., 2011a,b) . The complexity of AD pathology and etiology dictates to consider involvement of lipid rafts in its pathogenesis in a more generic way, not only as a simplistic link between cholesterol levels, amyloid burden and cognition. More important for normal brain functioning is to maintain lipid metabolism in the aging brain at its normal rate and integrity.