A protein known to exist in the brain for more than 30 years, called 5-lipoxygenase, has been found to play a regulatory role in the formation of the amyloid beta in the brain, the major component of plaques implicated in the development of Alzheimer's disease, according to researchers at Temple University's School of Medicine.
The researchers also found that inhibitors of this protein currently used to control asthma could possibly be used to prevent or treat Alzheimer's disease.
The researchers published their findings, "5-Lipoxygenase as Endogenous Modulator of Amyloid Beta Formation in Vivo," in the Annals of Neurology.
According to Domenico Pratic, an associate professor of pharmacology in Temple's School of Medicine and the study's lead researcher, the 5-Lipoxygenase enzyme is found in abundance mainly in the region of the brain, the hippocampus, involved in memory.
Pratic and his team discovered that 5-lipoxygenase, which unlike most proteins in the brain increases its levels during the aging process. It also controls the activation state of another protein, called gamma secretase, a complex of four elements which are necessary and responsible for the final production of the amyloid beta, a peptide that when produced in excess deposits and forms plaques in the brain. Today the amount of these amyloid plaques in the brain is used as a measurement of the severity of Alzheimer's.
"What we found was 5-lipoxygenase regulates and controls the amount of total amyloid beta produced in the brain," said Pratic. "With aging, the more 5-lipoxygenase you have the more amyloid beta you're going to produce. This will translate into a higher risk to develop full Alzheimer's"
A previous study by Pratic, in which researchers crossed a mouse model of Alzheimer's with a mouse that did not genetically feature 5-lipoxygenase, demonstrated that a lack of this enzyme protein alone can reduce the amount of disease in t
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