A new study from the Puglielli Lab opens a door to potential treatments for diseases of age, such as Alzheimer’s disease, by defining the roles of two enzymes that are imperative to protein production. “Endoplasmic reticulum acetyltransferases Atase1 and Atase2 differentially regulate reticulophagy, macroautophagy and cellular acetyl-CoA metabolism” was published in April in the journal Communications Biology.
Many diseases such as Alzheimer’s disease are known to be caused by a buildup of “bad proteins” within the cells. Sometimes when proteins are produced within a cell, they “misfold” and need to be disposed. In 2016, Puglielli proved that autophagy – or “one of the garbage disposal systems in the cell that gets rid of bad proteins or organelles” as Puglielli defines it – is regulated by the enzymes Atase1 and Atase2. The more efficient removal of such bad proteins allowed for the decrease of the symptoms associated with Alzheimer’s disease in mice.
In Puglielli’s present study, he focuses on the differences between these two enzymes in hopes of identifying one over the other as a potential therapy target. “In this work, we have shown that targeting Atase1 alone can help prevent Alzheimer’s disease in a mouse model,” says Puglielli, who is a professor in the Department of Medicine and an investigator at the Waisman Center and the Madison VA Medical Center. “This is helpful because it may allow us to target just one enzyme instead of both for therapeutic benefit in Alzheimer’s disease and other diseases of age.”
Continue reading this article: The Waisman Center published “The identities of enzymes: study further defines the function of a potential target for Alzheimer’s therapy” on April 20, 2021.
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