While researchers still have not found a cure for Alzheimer’s, the process that causes it to worsen, which includes the formation of plaques and inflammation, may be reversed. Researchers from Cedars Sinai Medical Center in Los Angeles have found a protein linked to high blood pressure that could induce an immune response against Alzheimer’s.
In Alzheimer’s development, peptide amino acids— called amyloid-beta— begin to form plaque in the brain, which then clog the space between nerve cells and inside blood vessels, blocking communication, and depleting a person’s memory. When the immune system tries to fight off the plaque, the condition worsens due to inflammation.
For this study, researchers looked at the enzyme— angiotensin-converting enzyme (ACE)— which is responsible for causing blood vessels to tighten, and how it may break down this plaque and prevent inflammation, along with other Alzheimer’s related problems. To test this, researchers genetically engineered lab mice to produce extra ACE in some immune cells, like macrophages and microglia. In addition, other lab mice were engineered to have amyloid plaques and Alzheimer’s symptoms. To the researchers’ surprise, the offspring of these mice performed similarly to normal mice in learning performance and memory tests.
Dr. Maya Koronyo-Hamaoui, assistant professor of neurosurgery in the Department of Neurosurgery and Department of Medical Sciences, said in a statement: “We were absolutely astonished by the lack of Alzheimer’s related pathology in the crossed mice … At first we thought we had a genotyping error in identifying these mice as carriers of the aggressive familial Alzheimer’s mutations. But we verified their genotypes and ran the experiments again and again, and confirmed the same findings.”
Having an abundance of ACE in these immune cells led to a “near-complete prevention” of cognitive decline. Although researchers were not fully sure of the means by which the ACE cleared amyloid plaque from blood vessels, “the enzyme has been found to break down longer amyloid peptides into shorter fragments that can more readily be ‘washed away’ or cleared from the system,” Koronyo-Hamaoui told Medical Daily in an email.
Researchers do not intend to increase levels of ACE in humans but say the most informative finding from the study “is the effectiveness of combining an approach to enhance the immune response with that of delivering inflammatory cells to enzymatically destroy beta-amyloid,” they wrote.