Angiotensin-converting enzyme, better known as a blood pressure lowering ACE inhibitor, is a naturally occurring protein found in tissues throughout the body. ACE inhibitors widen blood vessels by limiting activity of the AC enzyme. Recently, Cedars-Sinai scientists discovered that they could enhance immune response and attack beta-amyloid plaque in Alzheimer's by targeting this enzyme.
Multitudes of middle-aged and elderly people take ACE inhibitors to manage their blood pressure. The drug is considered safe when used as directed by the attending physician. This new study found that it is possible to genetically target certain immune blood cells to over produce the AC enzyme. This over production serves to break down defective proteins in the brain associated with Alzheimer’s disease. The process prevents cognitive decline in laboratory mice that are bred to model the disease, therefore the researchers are now convinced that high activity of the AC enzyme may, under the right circumstances, be beneficial.
Accumulation of beta-amyloid protein in the brain is believed to be associated with Alzheimer's disease by the majority of Alzheimer’s researchers. The theory is that protein levels and plaque deposits gradually build up, eventually damaging and destroying brain cells. This damage sets up an inflammatory process that is believed to add to the gradual decline of the affected person’s mental function.
Lead author of the study, Kenneth Bernstein M.D., along with his colleagues, medically engineered mice to over express the enzyme in macrophages, microglia and similar cells of their immune systems. It’s not yet been proven by scientists if the deposits result from an over production of beta-amyloid protein or from an inability of mechanisms, such as the immune system, to adequately clear it.
Regardless of the process, the most often accepted view is that any strategy that can reduce the amount of beta-amyloid protein in the brain early in disease process is likely to help prevent or slow the progression of Alzheimer’s.
Previous studies confirmed that ACE over expression could elevate immune responses against tumors and bacterial infections. This study identifies a novel role for the AC enzyme in the clearance of beta-amyloid in brain blood vessels, thus extending the findings to Alzheimer's.
The Cedars-Sinai study is published in the March issue of the Journal of Clinical Investigation. The authors said in the article that "while it is possible to envision a strategy for delivering ACE over expressing monocytes to patients, perhaps the most informative finding of our studies is the effectiveness of combining an approach to enhance the immune response with that of delivering inflammatory cells to enzymatically destroy beta-amyloid."
This study holds extra promise because, though it was still in trials with genetically engineered mice, it uses a drug already approved by the FDA for use in humans. That puts the research one step ahead of newly developed drugs being tested in clinical trials. Time will tell if these study results translate into a viable treatment for humans, but any time we can use already existing drugs in our fight against Alzheimer’s we gain time. As we all know, time is of the essence for those who have or are at risk for AD.
If you and/or a loved one would like to volunteer for an Alzheimer’s clinical trial, the National Institutes of Health (NIH) website for clinical trials can assist you. They help fund many clinical trials that looking that are for volunteers.
Medical News Today. (2014, February 5) Researchers enhance immune response and attack beta-amyloid plaque in Alzheimer's by targeting an enzyme that regulates high blood pressure. Retrieved from http://www.medicalnewstoday.com/releases/272123.php
Published On: March 04, 2014