A Protein Controlling Blood Pressure Can Enhance Immune Cells to Attack Alzheimer's Plaques
BrightFocus-funded research could lead to a new type of treatment
This research was supported by BrightFocus
The researchers found that genetically overproducing ACE in certain scavenging immune cells (called monocytes) that respond to inflammation helped to target and break down the toxic beta amyloid protein, and prevented cognitive decline in mice genetically engineered to show features of Alzheimer’s disease. Overexpression of ACE in just the immune cells had no effect on the blood pressure of the body. However, this brain beta-amyloid clean-up was prevented by giving the mice an ACE inhibitor drug, called ramipril, a type of blood pressure medication.
Therefore, it seems that the natural protein-busting capabilities of ACE, when present at high levels in the body’s blood stream, can have bad effects on blood pressure; however, when ACE is expressed at high levels in immune cells, it can have good effects on fighting plaque deposits in the brain.
What do these findings mean for patients with Alzheimer’s disease? There is much work that needs to be done before scientists can consider translating a potential strategy for delivering ACE-overexpressing monocytes to patients. However, these studies have demonstrated that a combination approach to treating Alzheimer’s, in this case increasing immune response to inflammation paired with delivery of a beta-amyloid-busting protein, might be the best way forward to reducing disease symptoms and improving cognitive function.
Amyloid is a general term for protein fragments that the body produces normally. Beta amyloid is a protein fragment snipped from an amyloid precursor protein (APP). In a healthy brain, these protein fragments are broken down and eliminated. In Alzheimer's disease, the fragments accumulate to form hard, insoluble plaques.