A recent study shows that a protein called ABCA7 plays a functional role as a potential biological link between cholesterol and inflammation in Alzheimer’s disease. The new work was published online August 25 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.
The findings demonstrate the sophisticated tuning and regulation of ABCA7 levels during inflammation and reduction of cholesterol availability. 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.
Domenico Praticò, MD, is the Scott Richards North Star Charitable Foundation Chair for Alzheimer’s Research, Professor and Director of the Alzheimer’s Center at Temple, and Professor of Pharmacology at the Lewis Katz School of Medicine at Temple University