As cholesterol is integral to ordered lipid rafts, the consequences of cholesterol depletion are widely regarded as effects of raft disruption (Hao et al., 2001; Mondal et al., 2009) . In this context the cholesterol content in the membranes has an inversely proportional relationship with the membrane-perturbing effects of Aβ oligomers (Cecchi et al., 2009 ). As such, if cholesterol increases do elevate lipid raft abundance, then it would increase Aβ formation (Simons et al., 1998; Ehehalt et al., 2003) and, on the contrary, low cholesterol levels will lead to up-regulation of the activity of the α-secretase, ADAM10 (Kojro et al., 2001) . Cholesterol depletion in cells by MβCD was shown to affect APP-processing and formation of functionally active AICD resulting in reduced levels of expression of the amyloid-degrading enzyme, neprilysin (Belyaev et al., 2010) . On the other hand, cholesterol has been shown to bind C99, which promotes amyloidogenic processing (Beel et al., 2010) and the increase of Aβ levels, in turn, can cause changes in cholesterol homeostasis in the Golgi and plasma membrane ). Formation of the Aβ "seed" and initiation of Aβ aggregation was also shown to be cholesterol dependent (Mizuno et al., 1999; Kakio et al., 2001; Simons et al., 2001) . In a more biophysical sense, raised cholesterol has been implicated in facilitating the insertion of Aβ into the plasma membrane. In so doing, Aβ then destroys the cells' membrane integrity (Ji et al., 2002) .