• Aggregation;
  • Alzheimer’s disease;
  • amyloid β-protein;
  • oligomerization;
  • synaptic dysfunction


Converging lines of evidence suggest that progressive accumulation of the amyloid β-protein (Aβ) plays a central role in the genesis of Alzheimer’s disease, but it was long assumed that Aβ had to be assembled into extracellular amyloid fibrils to exert its cytotoxic effects. Over the past decade, data have emerged from the use of synthetic Aβ peptides, cell culture models, β-amyloid precursor protein transgenic mice and human brain to suggest that pre-fibrillar, diffusible assemblies of Aβ are also deleterious. Although the precise molecular identity of these soluble toxins remains unsettled, accumulating evidence suggests that soluble forms of Aβ are indeed the proximate effectors of synapse loss and neuronal injury. Here we review recent progress in understanding the role of soluble oligomers in Alzheimer’s disease.