UCSB researchers have discovered that certain compounds in cinnamon may have the potential to be used in the development of a drug that would prevent Alzheimer’s disease.

According to graduate student Roshni George, who worked alongside adjunct biology professor Donald Graves and associate professor John Lew of the Department of Molecular, Cellular and Developmental Biology, cinnamon contains two compounds — cinnamaldehyde and epicatechin — that obstruct the aggregation of a protein called tau, which is responsible for the assembly of microtubules in brain cells, but can also lead to the development of neuronal “tangles.” In warding off the development of these “tangles,” the effects of Alzheimer’s disease can be thrown off. The researcher team has published their study, “Interaction of Cinnamaldehyde and Epicatechin with Tau: Implications of Beneficial Effects in Modulating Alzheimer’s Disease Pathogenesis,” in the Journal of Alzheimer’s Disease.

In a previous study, the researchers found that an aqueous extract of cinnamon could inhibit the aggregation of tau and even reverse the effects of Alzheimer’s by inducing dissociation of tangles. The current study was devoted to carrying out more detailed investigations of the effects of cinnamaldehyde and epicatechin.

According to George, inhibiting the aggregation of tau is crucial to preventing Alzheimer’s.

“Aggregation of tau that occurs inside neurons is one of the hallmarks of Alzheimer’s disease, so inhibiting this process would potentially protect the neurons and prevent neuronal dysfunction that occurs in Alzheimer’s disease and aging,” George said in an email.

Cinnamaldehyde, the compound responsible for the bright and sweet smell of cinnamon, protects tau from oxidative stress, which is the result of increased cellular production of free radicals and inability of antioxidants to neutralize them.

“The transient binding of these compounds to the cysteines acts as a cap that protects them from these modifications and in this sense keeps tau from aggregating,” George said.

Epicatechin — an antioxidant that also present in blueberries, chocolate and red wine — acts as a cap on cysteines as well, although it is also activated by oxidation.

“Epicatechin can itself become oxidized,” George said. “It is the oxidized epicatechin that can then interact with tau cysteines in a protective manner.”

George also said oxidation of cell membranes produces reactive byproducts, such as the protein Acrolein, which binds to cysteine residues and leads to aggregation. While this process is irreversible, cinnamaldehyde and epicatechin may still prevent Alzheimer’s disease.

“What we show is that cinnamaldehyde and epicatechin can directly protect tau from being modified by oxidative stress, or indirectly by acting as an antioxidant or trapping the toxic byproducts that could modify tau,” George said.

According to Xuemei Zhang, assistant specialist for professor of neuroscience Kenneth Kosik’s Molecular and Cellular Neurobiology Lab, more research is needed to develop a preventative drug for Alzheimer’s.

“Right now, the problem is the treatment,” Zhang said. “There is no treatment that has shown in clinical trials to have a therapeutic effect.”

Current research, Zhang said, focuses on reducing the effects of oxidative stress and researchers must first optimize the structure of the compound in pharmacogenetic studies and then figure out how it is metabolized in pharmacodynamic studies.

Chair of the Department of Molecular, Cellular and Developmental Biology William Smith said research is promising, but he said it may still take more time before reaching the development phase of treatment medicines.

“It’s important to be cautious about this,” Smith said. “If you look at the study, it’s really very, very preliminary.”

Smith also warned against eating too much cinnamon, which is obtained from the bark of the cinnamon tree and thus contains trace amounts of other compounds that can lead to illness when consumed in large quantities. Additionally, Smith said cinnamaldehyde and epicatechin would need to be concentrated in the form of a drug to elicit any real effect.

“It doesn’t mean that you should go to the grocery store and start eating cinnamon,” Smith said.

Furthermore, Smith said a new medicine created out of the study’s findings would have treatment abilities that rival current medicines.

“Unlike some of the treatments out there — which may delay the onset — this has the potential to reverse the damage,” Smith said. “We’re very proud to have this discovery come out of the department.”

A version of this article appeared on page 5 of May 30th’s print edition of the Daily Nexus.