“…The amyloid hypothesis has undergone several modifications, mainly concerning the type of A thought to cause AD: initially this was the amyloid plaque, followed by increased concentrations of A 42 , then increased A 42 : A 40 ratio, and finally oligomeric A [2]. Results from clinical trials have shown that removing plaques will not reverse the damage or stop AD [3,4]. Recent evidence suggests that this toxicity may be linked to the aggregation state of the peptide, implicating oligomers, rather than insoluble fibrils, as the primary toxic species [5,6].…”