Recently two novel mechanisms linking gangliosides with AD have been described by Grimm et al. (2012b) . They discovered that Aβ binds to GD3-synthase (GD3S, the key-enzyme in converting a-series gangliosides to major brain specific b-series) and inhibits its activity. On the other hand, the APP intracellular domain AICD, together with Fe65, was found to down-regulate expression of the GD3S gene. This provides an explanation for age-dependent and AD-related changes in brain ganglioside patterns and supports an essential role of APP in ganglioside homeostasis. Another link between gangliosides and AD lies in their ability to alter APP processing. As observed by the authors, GM3 was able to decrease production of Aβ while GD3 was shown to increase its levels in COS7 cells. This might be related to the changes in the properties of lipid rafts containing different amounts of GM3 or GD3 ganglioside species and their ability to regulate activity of βand γ-secretases.