|PETERSON, DYLAN - University Of California|
|GEORGE, ROSHINI - University Of California|
|LAPOINTE, NICOLE - University Of California|
|GRAVES, D - University Of California|
|LEW, JOHN - University Of California|
Submitted to: Journal of Alzheimer's Disease
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/5/2009
Publication Date: 5/11/2009
Citation: Peterson, D.W., George, R.C., Scaramozzino, F., Lapointe, N.E., Anderson, R.A., Graves, D.J., Lew, J. 2009. Cinnamon extract inhibits tau aggregation associated with Alzheimer’s Disease in vitro. Journal of Alzheimer's Disease. 17(3):585-597.
Interpretive Summary: As many as 5 million Americans are living with Alzheimer’s disease. Alzheimer's destroys brain cells, causing problems with memory, thinking, and behavior severe enough to affect work, lifelong hobbies or social life. Alzheimer’s gets worse over time, and it is fatal. Today it is the sixth-leading cause of death in the United States. We determined the effects of adding a water extract of cinnamon on two factors that are hallmarks of Alzheimer’s disease: tau aggregation and filament formation. The cinnamon extract caused complete disassembly of tau filaments and substantial alteration of the arrangement of filaments in the cells taken from the brain of people who had died with Alzheimer’s disease. This work suggests that compounds in cinnamon may be beneficial to the prevention and/or alleviation of some of the symptoms of Alzheimer’s disease, although since the study was done with isolated cells, whether a similar finding would occur in patients consuming cinnamon or its extract is unknown. This study will be of benefit to scientists working on the causes and prevention of Alzheimer’s disease.
Technical Abstract: An aqueous extract of Ceylon cinnamon (C. zeylanicum) was found to inhibit tau aggregation and filament formation, hallmarks of Alzheimer’s disease (AD) in vitro using brain cells taken from patients who died with AD. The extract also promoted complete disassembly of recombinant tau filaments, and caused substantial alteration of the morphology of paired-helical filaments isolated from AD brain. Cinnamon extract 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 remaining inhibitory activity could be attributed to cinnamaldehyde. This work shows that compounds endogenous to cinnamon may be beneficial to Alzheimer’s disease themselves, or it may guide the discovery of other potential therapeutics once the mechanisms of action can be discerned.