Turmeric Derived Compound Neuroprotective Against Stroke

A synthetic derivative of the curry spice turmeric dramatically improves the behavioral and molecular deficits seen in animal models of ischemic stroke and traumatic brain injury (TBI). Two studies suggest that the turmeric compound may have clinical promise for these conditions, which currently lack good therapies.

Ischemic stroke is the leading cause of disability and the third leading cause of death of older people in the United States, while TBI is the leading cause of death and disability in both civilians and military personnel under the age of 45; in particular, it is the major cause of disability in veterans returning from Iraq and Afghanistan. In both conditions, those who survive frequently have serious behavioral and memory deficits. The only FDA-approved treatment for stroke is tissue plasminogen activator (TPA), which is effective only in about 20 percent of cases. There is no clinically documented treatment for TBI.

In earlier studies, the researchers had developed a series of new compounds using a novel drug discovery paradigm that starts with natural products derived from plants; it then calls for selecting synthetic derivatives that show efficacy in multiple assays testing protection against various aspects of the nerve cell damage and death that occur in brain injuries and in age-associated neurodegenerative diseases. One compound, called CNB-001, which was derived from curcumin, the active ingredient in the spice turmeric, proved highly neuroprotective in all of the assays; it also enhanced memory in normal animals.

Employing the same animal model of stroke that was used to develop TPA, this study showed that the turmeric compound was at least as effective as TPA in preventing the behavioral deficits caused by stroke. The study also demonstrated that unlike TPA, which reduces clotting in the blood vessels of the brain, the turmeric compound has a direct protective effect on nerve cells within the brain. It was also found that it maintains specific cell signaling pathways required for nerve cell survival.

In another study researchers used a rodent model of TBI to demonstrate that CNB-001 dramatically reversed the behavioral deficits in both locomotion and memory that accompany the brain injury. As with stroke, CNB-001 was again found to maintain the critical signaling pathways required for nerve cell survival, as well as the connections between nerve cells that are lost with the injury.

The results of these two studies, which used two distinct models of brain injury, indicate that the turmeric compound has clinical potential in conditions where there is currently no effective treatment.

“Existing drug therapies for complex neurological conditions such as stroke and Alzheimer’s disease target only one aspect of the condition, while in fact many different factors contribute to the pathology,” observes Schubert. “In the drug discovery program our lab uses at Salk, drug candidates must show efficacy in tissue culture models of several aspects of the condition before they are introduced into animal models. We believe that this approach is making an important difference in the discovery of effective drugs.”

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