Affiliations: [a] Department of Molecular, Cellular, and Developmental Biology, University of California, Santa Barbara, CA, USA | [b] Beltsville Human Nutrition Center, Beltsville, MD, USA
Correspondence:
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Corresponding author: John Lew, Department of Molecular, Cellular and Developmental Biology, University of California, Santa Barbara, CA 93106, USA. Tel.: +1 805 893 5336; Fax: +1 805 893 2212; E-mail: lew@lifesci.ucsb.edu.
Note: [1] These authors contributed equally.
Abstract: An aqueous extract of Ceylon cinnamon (C. zeylanicum) is found to inhibit tau aggregation and filament formation, hallmarks of Alzheimer's disease (AD). The extract can also promote complete disassembly of recombinant tau filaments and cause substantial alteration of the morphology of paired-helical filaments isolated from AD brain. Cinnamon extract (CE) was not deleterious to the normal cellular function of tau, namely the assembly of free tubulin into microtubules. An A-linked proanthocyanidin trimer molecule was purified from the extract and shown to contain a significant proportion of the inhibitory activity. Treatment with polyvinylpyrolidone effectively depleted all proanthocyanidins from the extract solution and removed the majority, but not all, of the inhibitory activity. The remainder inhibitory activity could be attributed to cinnamaldehyde. This work shows that compounds endogenous to cinnamon may be beneficial to AD themselves or may guide the discovery of other potential therapeutics if their mechanisms of action can be discerned.
Keywords: Aggregation, Alzheimer's disease, cinnamaldehyde, cinnamon extract, filaments, proanthocyanidin, tau
