Orally administrated cinnamon extract reduces ?-amyloid oligomerization and corrects cognitive impairment in Alzheimer's disease animal models.

ABSTRACT: An increasing body of evidence indicates that accumulation of soluble oligomeric assemblies of ?-amyloid polypeptide (A?) 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 A? plaque formation by compounds from natural sources. Yet, evidence for the ability of common edible elements to modulate A? oligomerization remains an unmet challenge. Here we identify a natural substance, based on cinnamon extract (CEppt), which markedly inhibits the formation of toxic A? oligomers and prevents the toxicity of A? 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 A? in their brain. Furthermore, oral administration of CEppt to an aggressive AD transgenic mice model led to marked decrease in 56 kDa A? oligomers, reduction of plaques and improvement in cognitive behavior. Our results present a novel prophylactic approach for inhibition of toxic oligomeric A? species formation in AD through the utilization of a compound that is currently in use in human diet.

SUBMITTER: Frydman-Marom A 

PROVIDER: S-EPMC3030596 | biostudies-literature | 2011 Jan

REPOSITORIES: biostudies-literature