Frydman-Marom_2011_PLoS.One_6_e16564

An increasing body of evidence indicates that accumulation of soluble oligomeric assemblies of beta-amyloid polypeptide (Abeta) play a key role in Alzheimer's disease (AD) pathology. Specifically, 56 kDa oligomeric species were shown to be correlated with impaired cognitive function in AD model mice. Several reports have documented the inhibition of Abeta plaque formation by compounds from natural sources. Yet, evidence for the ability of common edible elements to modulate Abeta oligomerization remains an unmet challenge. Here we identify a natural substance, based on cinnamon extract (CEppt), which markedly inhibits the formation of toxic Abeta oligomers and prevents the toxicity of Abeta on neuronal PC12 cells. When administered to an AD fly model, CEppt rectified their reduced longevity, fully recovered their locomotion defects and totally abolished tetrameric species of Abeta in their brain. Furthermore, oral administration of CEppt to an aggressive AD transgenic mice model led to marked decrease in 56 kDa Abeta oligomers, reduction of plaques and improvement in cognitive behavior. Our results present a novel prophylactic approach for inhibition of toxic oligomeric Abeta species formation in AD through the utilization of a compound that is currently in use in human diet.