An innovative strategy to lessen the plaques was also found in the study.
Alzheimer’s-Associated Plaques ,The oral administration of rapamycin to an Alzheimer’s disease mouse model induces an increase in beta (β)-amyloid protein plaques, according to researchers from The University of Texas Health Science Center at San Antonio (UT Health San Antonio). β-amyloid buildup is a hallmark of Alzheimer’s disease. Rapamycin is FDA-approved for the treatment of transplant and cancer patients. The drug is also referred to as sirolimus and is sold under the name Rapamune. Publicly available data suggest that the drug might also improve learning and memory in aged mice. According to publicly accessible evidence, the medication may also boost learning and memory in elderly mice. The UT Health San Antonio researchers, on the other hand, discovered that following rapamycin administration, a protein called Trem2 (triggering receptor expressed on myeloid cells 2) is drastically reduced. Trem2 is found in microglia, immune cells found in the brain and spinal cord.
Alzheimer’s-Associated Plaques , “Trem2 is a receptor located on the surface of the microglia, and it enables these cells to engulf and degrade β-amyloid,” said study senior author Manzoor Bhat, Ph.D. “Loss of Trem2 in microglia impairs the vital function of amyloid degradation, which in turn causes a buildup of β-amyloid plaques.” Dr. Bhat is professor and chairman of the Department of Cellular and Integrative Physiology at UT Health San Antonio and vice dean for research in the university’s Joe R. and Teresa Lozano Long School of Medicine.
Source: This news is originally published by scitechdaily