The protein known as ABCA7 serves as a functional element, potentially bridging the biological connection between cholesterol and inflammation in Alzheimer’s disease. The new work was published online in the journal Cells.

With research performed at the Alzheimer’s Center at Temple University (ACT), under the leadership of Domenico Pratico, M.D., Director of ACT, and Nicholas Lyssenko, Ph.D., the paper reports on the effects of cholesterol depletion and inflammation on ABCA7, a cellular transporter that regulates the way molecules pass through cell membranes.

ABCA7’s Role in Lipid Removal: A Crucial Process to Prevent Neurodegeneration

The authors suggest that removal of lipids accumulated in neural cells may be a routine action of ABCA7, which, if not performed, can lead to neurodegeneration. Additionally, the study suggests that a loss of ABCA7 in Alzheimer’s Disease could occur either because of a sudden change in cholesterol, or because of inflammation onset in microglia and astrocytes, which are neuronal supporting cells.

Previous work showed that ABCA7 levels in the brain decline with aging, and mutations that cause a loss of its function are reported in Alzheimer’s Disease patients. The current study provides new clues on the role of ABCA7 in Alzheimer’s Disease, suggesting it could be exploited for the development of new treatments.