Taking into account the important role of gangliosides in normal brain function, their involvement in the pathogenesis of AD should be treated with caution since different species of gangliosides will have a different impact on the integrity and properties of neuronal membranes. Recently, by using G3 synthase KO mice (lacking only b-series gangliosides) and GM2/GD2 synthase KO mice (which lack almost all gangliosides except GM3 and GD3) it was found that these ganglioside species are important for neuroprotection and anti-inflammatory response via maintenance of lipid rafts . Intraventricular treatment of AD patients with GM1 was shown to stop the progression of cognitive deterioration and improve motor performance and neuropsychological assessments (Svennerholm et al., 2002) . Peripheral utilization of GM1 for prevention of Aβ aggregation in the brain via establishing peripheral/brain dynamics of Aβ was suggested as a possible therapeutic approach for AD since in the PS/APP mice this was shown to reduce Aβ accumulation in the brain (Matsuoka et al., 2003) . However, due to the antigenic properties of gangliosides this might provoke some side-effects (López-Requena et al., 2007) .