Two new studies suggest that a compound derived from turmeric may have clinical promise for ischemic stroke and traumatic brain injury (TBI), both of which currently lack good therapies.
A synthetic derivative of turmeric made by scientists at the Salk Institute for Biological Studies dramatically improved the behavioral and molecular deficits seen in animal models of these conditions.
In previous studies, David R. Schubert and Pamela Maher in the Salk Cellular Neurobiology Laboratory 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.
While the Salk group has a great deal of expertise in age-associated neurological diseases such as Alzheimer's, they do not run animal models of TBI and stroke.
"To test the prediction that drugs from our new drug discovery scheme will work in multiple models of CNS disease and trauma," Schubert explained, "we undertook a series of experiments to assay the drugs in collaboration with researchers at Cedars- Sinai and UCLA, who are leaders in the fields of stroke and TBI, respectively, and appreciate the potential for therapeutics based on natural products and their derivatives."
Employing the same animal model of stroke that was used to develop TPA [tissue plasminogen activator, a treatment for stroke], Paul Lapchak, of the Department of Neurology at the Burns and Allen Research Institute at Cedars-Sinai Medical Center in Los Angeles, collaborated with Schubert's team in a study that showed that CNB- 001 was at least as effective as TPA in preventing the behavioral deficits caused by stroke.
The study, published in the December 2, 2010 edition of the Journal of Neurochemistry, also demonstrated that unlike TPA, which reduces clotting in the blood vessels of the brain, the Salk compound has a direct protective effect on nerve cells within the brain. Maher has found that it maintains specific cell signaling pathways required for nerve cell survival.
Similarly, in a study to be published in early 2011 in Neurorehabilitation and Neural Repair, Fernando Gomez-Pinilla and his colleagues in the Department of Physiological Science and Division of Neurosurgery at the University of California, Los Angeles 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.
