Aβ-ganglioside interactions in the pathogenesis of Alzheimer's disease

It is widely accepted that the abnormal self-association of amyloid beta-protein (A beta) is central to the pathogenesis of Alzheimer's disease, the most common form of dementia. Accumulating evidence, both in vivo and in vitro, suggests that the binding of A beta to gangliosides, especially monosialoganglioside GM1, plays an important role in the aggregation of A beta. This review summarizes the molecular details of the binding of A beta to ganglioside-containing membranes and subsequent structural changes, as revealed by liposomal and cellular studies. Furthermore, mechanisms of cytotoxicity by aggregated A beta are also discussed.