Scientists at Dana-Farber Cancer Institute report found such as the brain a system switches designed to protect its neurons of toxic "free radicals", a waste product of cellular metabolism, which involved degenerative brain disease, heart attacks, strokes, cancer and aging. Potentially, the researchers say, can it strengthen drug use, Alzheimer's, Huntington's and possibly other maladies anti including system in the brain as a treatment for currently incurable diseases such as Parkinson, possible. Dana-Farber's Bruce Spiegelman, PhD, and colleagues, with a mouse model discovered that a regulatory protein, PGC 1a changes on anti including system when free radicals or reactive oxygen species start to accumulate. It is believed that some brain diseases include a failure of the protective device, and the authors report that turn on PGC 1a high concentrations in cultured cells against nerve toxins protected. Results are reported in the Oct. 20 issue of the journal cell. "This could have broad implications for many diseases which species involved reactive oxygen," Spiegelman said. Antioxidant food supplements with some success were used in patients with neurodegenerative diseases but Spiegelman "is found the process triggered by PGC 1a as nature does it." Researchers are currently screening drugs looking for connections that could encourage expression in brain cells PGC 1a, explore whether any harmful side effects could result. PGC-1a is a transcriptional Coactivator Spiegelman's Dana-Farber lab discovered in 1998. It was later found a master is regulatory role in metabolic processes and muscle function as a perpetrator in diabetes. Sets the report for the first time that PGC 1a both drives the mitochondria energy to make and throws the cleanup of toxic free radicals to that accumulate in the cell as by-products. How excess free radicals build placed their toxicity that cell under "oxidative stress" prompts, the cell to another PGC-1a, to produce, which in turn drives the anti including defenses in action. "With this mechanism, which can speed body mitochondrial education and at the same time suppress the creation of reactive oxygen species are known be harmful terribly on the cell," Spiegelman, explains the Professor of cell biology at Harvard Medical School. In this respect, the cell with a self-cleaning oven - but one that becomes less efficient, with age and certain diseases could be compared. Therefore the new identification of a specific regulator of the body's own anti including system could lead to more effective treatments for a range of diseases and possibly some delay, the effects of aging, the researchers say. Spiegelman and other mice had raised in previous experiments, the pkg-1a gene lacked. As would be expected, the absence of the pkg-1a caused the mice anomalies in your metabolism to fulfilling - had less exercise capacity and were very sensitive to the cold. But what the scientists had predicted was not that the mice neurodegenerative lesions in their brains and behaved unusually: that was an idea, that the cells "self-cleaning" mechanism without right, PGC 1a was not enabled the mice leave more susceptible for brain damage from breakaway free radicals. Is made of current research Spiegelman and his colleagues normal mice and rodents a nerve toxin that accelerates the production of free radicals missing PGC 1a. Mice without PGC 1a suffered more brain damage, because you enable your anti including defence mechanisms could not. Finally, caused, to examine whether increasing PGC 1a activity in the brain against oxidative stress protect mouse brain cells and human brain cells in the laboratory to 40 times more pkg-1a than normal scientists would. Made available the cells to increasing amounts of paraquat or hydrogen peroxide, chemicals that cause oxidative stress and cell damage. The result: many more brain cells survived the attack to supplement as cells without the additional PGC 1a activity to your defense. PGC 1a is now shown to suppress both rev up energy production in the mitochondria and the resulting free radicals, wrote "this is an almost ideal protein to control or limit the damage in neuro-degenerative diseases, the defective mitochondrial function were seen associated with" the authors. As a result, find drugs increase the PGC 1a in the brain "could represent a new mode of therapy for a number of diseases, which are both common and have marginal therapies at this moment." Lead authors of the report are Julie St-Pierre, PhD, and Stavit Drori, PhD, formerly of Dana-Farber and Harvard Medical School. Deaconess Medical Center and Harvard Medical School based the paper of the co-authors of the Dana-Farber, Beth Israel. Research funded by the national institutes of health part. Dana-Farber Cancer Institute (http://www.dana-farber.org/) is a principal teaching affiliate of Harvard Medical School and among the leading cancer research and care centers in the United States. It is a founding member at the Dana-Farber/Harvard Cancer Center (DF/HCC), designated a comprehensive cancer center of National Cancer Institute.
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