NIH Research Festival
Alzheimer's Disease (AD) is a prevalent cause of dementia, affecting approximately 6.7 million individuals aged 65 and above in the United States, with no effective cure currently available. While our understanding of the immune system's role in central nervous system diseases is advancing, the involvement of lymphocytes, specifically CD8+ T cells, remains incompletely understood. In our recent investigation, we utilized immunohistochemical and flow cytometry techniques to examine mouse models of Alzheimer's Disease, namely the 5xFAD and APPSAA models known for their formation of amyloid beta plaques, a hallmark of AD in humans.
Through our study, we observed a significant increase in CD8+ T lymphocytes, a population of cytotoxic immune cells, in aged and AD-like mice. Moreover, we demonstrated that inhibiting the development of CD8+ T cells in these mice, achieved by deleting beta-2 microglobulin (B2m), led to improved memory and reduced plaque load. To gain a deeper understanding of the specific contributions of CD8+ T cells in AD pathology, we are currently utilizing a depletion antibody to target and eliminate CD8+ T cells in AD-like mice.
Our hypothesis suggests that this intervention may provide a means to rescue or prolong memory in these mice, potentially unveiling novel therapeutic avenues for AD. By further exploring the impact of CD8+ T cells on AD progression, we aim to enhance our comprehension of the disease mechanisms and identify potential targets for therapeutic intervention.
Scientific Focus Area: Neuroscience
This page was last updated on Monday, September 25, 2023