A drug used to treat asthma has been shown, in a transgenic mouse model, to help reduce the formation of amyloid beta, a peptide in the brain that is implicated in the development of Alzheimer's disease, according to researchers at Temple University's School of Medicine. The researchers published their findings, "Pharmacologic Blockade of 5-Lipoxygenase Improves the Amyloidotic Phenotype of an AD Transgenic Mouse Model," in the American Journal of Pathology. In previous studies, the Temple researchers discovered that 5-lipoxygenase, an enzyme long known to exist in the brain, controls the activation state of gamma secretase, another enzyme that is necessary and responsible for the final production of amyloid beta. When produced in excess, amyloid beta causes neuronal death and forms plaques in the brain. The amount of these amyloid plaques in the brain is used as a measurement of the severity of Alzheimer's. In the current study, led by Dr. Domenico Praticò, an associate professor of pharmacology in Temple's School of Medicine, the researchers tested the drug Zileuton, an inhibitor of 5-lipoxygenase typically used to treat asthma, in a transgenic mouse model of Alzheimer's disease. At the end of the treatment they found that this drug, by blocking the 5-lipoxygenase, reduced gamma secretase's production of amyloid beta and the subsequent build up of amyloid plaques in the brain by more than 50 percent. Dr. Praticò said that gamma secretase is present throughout the body and, despite its role in the development of amyloid plaques, plays a significant role in numerous important functions. Direct inhibitors of gamma secretase are known, he said, but blocking the enzyme completely may cause problems such as the development of cancer.
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