In Alzheimer's disease condition, the control and adjustment of ABCA7 levels in response to inflammation and the decrease in the availability of cholesterol.
The protein known as ABCA7 serves as a functional element, potentially bridging the biological connection between cholesterol and inflammation in Alzheimers disease. The new work was published online in the journal Cells. (1✔ ✔Trusted Source
Down-Regulation of ABCA7 in Human Microglia, Astrocyte and THP-1 Cell Lines by Cholesterol Depletion, IL-1β and TNFα, or PMA
Go to source) 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.‘Elevated cholesterol levels and persistent, long-term inflammation are believed to be potential factors that raise the likelihood of developing Alzheimer's disease. #dementia #alzheimersdisease #cholesterol #worldalzheimersday’
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. Reference:
- Down-Regulation of ABCA7 in Human Microglia, Astrocyte and THP-1 Cell Lines by Cholesterol Depletion, IL-1β and TNFα, or PMA - (https://www.mdpi.com/2073-4409/12/17/2143)