A drug that jams a key enzyme regulating cholesterol drastically reduces the levels of brain-clogging amyloid plaque in mice engineered to have a human form of the amyloid protein. According to Dora Kovacs and her colleagues, the findings suggest that such inhibiting drugs could be used to treat and prevent Alzheimers disease (AD).
CP-113,818 mimics a cholesterol molecule that the enzyme, called "acyl-coenzyme A: cholesterol acyltransferase" (ACAT), converts into a form of cholesterol that the cell stores in droplets. When CP-113,818 is administered, it plugs into the "active site" of ACAT, jamming its operation and preventing the enzyme from processing cholesterol.
Cholesterol is required in the production of the short protein called Aß peptide, the building block for the amyloid plaque that clogs the brain in Alzheimers disease, ultimately killing brain cells. In the mouse experiments, the researchers administered CP-113,818 by implanting slow-release biopolymer pellets under the skin of both normal mice and transgenic animals engineered to have the human form of the aberrant protein that leads to Aß peptide. Such transgenic mice develop the hallmark pathology of Alzheimers, including brain amyloid plaque and memory deficits.
Heidi Hardman | EurekAlert!
The dense vessel network regulates formation of thrombocytes in the bone marrow
25.07.2017 | Rudolf-Virchow-Zentrum für Experimentelle Biomedizin der Universität Würzburg
Fungi that evolved to eat wood offer new biomass conversion tool
25.07.2017 | University of Massachusetts at Amherst
21.07.2017 | Event News
19.07.2017 | Event News
12.07.2017 | Event News
25.07.2017 | Physics and Astronomy
25.07.2017 | Earth Sciences
25.07.2017 | Life Sciences