A new study has found that curry, a common and popular cooking additive, could be an effective enhancer of an enzyme that protects the
brain against oxidative conditions. This research is an important first step in determining whether curry could be preventive agent against acute neurodegenerative conditions, or reducing the progression of chronic and age associated
neurodegenerative disorders, such as Alzheimer’s disease.
Free Radicals and Neurodegenerative Disease
One of the most prominent current theories of aging is the "free radical theory." According to this theory, free radical molecules generated through mitochondrial metabolism can act as causative factor of abnormal function and cell death. Various toxins in the environment can injure mitochondrial enzymes, leading to increased generation of free radicals and oxidative stress, that over the life-span would eventually play a major role in aging. Free radical’s oxidative damage to key intracellular targets such as DNA or proteins has been shown to be a major cause of the degenerative diseases related to aging such as cancer and Alzheimer’s disease.
Luckily, mammalian cells have developed highly protective systems against including oxidative challenges over time. When properly activated, each one of these cell systems has the possibility to restore cellular homeostasis and resume the ability to fight off oxidation. Activation of antioxidant pathways is particularly important for tissue with relatively weak antioxidant defenses, such as the brain. In fact, increasing evidence points to the notion that reduced cellular expression and activity of antioxidant proteins and the consequent oxidative stress are fundamental causes for brain aging processes and neurodegenerative diseases.
HO-1 and Curcumin
There are a variety of genes encoding proteins that possess anti-oxidant properties. Of particular interest in the central nervous system (CNS) is the hemeoxygenase-1 (HO-1), which has been reported to operate as a fundamental defensive mechanism for neurons exposed to an oxidant challenge.
At the same time, a number of studies have supported the beneficial effects of some commonly used natural products in preventing various pathologic conditions. Spices and herbs often contain phenolic substances with potent antioxidative and chemopreventive properties. Among them is curcumin, a natural phenolic agent, extracted from the rhizome of Curcuma Longa, and the yellow pigment in curry, strongly induced HO-1 expression and activity in rat astrocytes.
In recent years, there has been an unprecedented interest in identifying new pharmacological strategies to increase defense mechanisms by activating multiple antioxidant defense genes, a process that has been referred to as programmed cell life. Previous studies have shown that induction of HO-1 can represent an efficient antioxidant system and a potential pharmacological target in a variety of oxidant- and inflammatory-mediated diseases, including brain aging and neurodegenerative disorders.
A New Study
A new study extends previous findings examining the neuroprotective effects of curcumin and its ability to induce HO-1 on cultured hippocampal neurons. This research effort investigated the effects of curcumin on the expression profiles of other genes involved in the cellular stress response. The study also explored subcellular localization of HO-1 protein in one of the large cells of nervous tissue after treatment with curcumin.
The investigators of a study entitled "Curcumin Cytoprotective Effect in Rat Astrocytes and Neurons is Mediated by Specific Induction of HO-1," will present their findings at the American Physiological Society’s (APS) (http://www.the-aps.org) annual scientific conference, Experimental Biology 2004, being held April 17-21, 2004, at the Washington, D.C. Convention Center. The research team represents two countries. The Italian researchers are Giovanni Scapagnini from the Institute of Neurological Sciences, CNR, Catania, Claudia Colombrita and Vittorio Calabrese at the Dipartimento di Scienze Chimiche, Universita' di Catania, and Alessia Pascale, at the Department of Experimental and Applied Pharmacology, Universita' di Pavia, Pavia. In the United States, the researchers are Michael L. Schwartzman and Nader G. Abraham from the Department of Pharmacology, New York Medical College, Valhalla, NY.