In a recent study, scientists from St. Jude Children’s Research Hospital have found a subset of immune cells that can slow down the progression of Alzheimer’s disease, a condition known for causing memory loss and cognitive decline.
This groundbreaking research, published in Nature Immunology, reveals how these immune cells interact with protein aggregates, known as beta-amyloid plaques, which are a hallmark of Alzheimer’s.
Alzheimer’s disease currently affects approximately 5.8 million Americans. It is a neurodegenerative condition that progressively impairs cognitive functions, particularly memory.
The formation of beta-amyloid plaques in the brain is a key factor contributing to the disease’s progression. However, the new study offers hope by uncovering the role of certain immune cells in combating this process.
Co-first author Jordy Saravia, Ph.D., from St. Jude Department of Immunology, highlights the growing interest in the role of the immune system in neurodegenerative diseases.
The research team focused on microglia, the brain’s immune cells, which are typically responsible for clearing beta-amyloid plaques.
In Alzheimer’s, microglia can lose their capacity to remove these plaques and may even exacerbate their progression by releasing inflammatory substances.
The researchers discovered that a specific subtype of immune cells, called CD8+ T cells, plays a crucial role in slowing the accumulation of beta-amyloid plaques.
These cells interact with microglia, helping to limit the beta-amyloid burden and preserve memory functions in a mouse model of Alzheimer’s.
Co-first author Wei Su, Ph.D., also from St. Jude Department of Immunology, explained that this is the first study to demonstrate that CD8+ T cells can be protective in a model of Alzheimer’s disease.
The findings could pave the way for new interventions in treating neurodegenerative diseases.
The study also found that the protective role of CD8+ T cells is mediated by a protein on their surface, called CXCR6, which interacts with the protein CXCL16 expressed by microglia.
This interaction, likened to a molecular handshake, is crucial for the CD8+ T cells to effectively communicate with microglia and regulate their function.
When the researchers removed the gene for CXCR6 in the CD8+ T cells, the mice developed more severe Alzheimer’s symptoms.
This was partially because the CD8+ T cells without CXCR6 could not accumulate in the brain near the microglia or the plaque sites, nor could they acquire the right function to suppress inflammation.
Corresponding author Hongbo Chi, Ph.D., emphasized the need for a better understanding of these neuro-immune interactions to improve outcomes for Alzheimer’s disease.
The study not only highlights the importance of CD8+ T cells in maintaining brain homeostasis but also pinpoints the central role of the protein CXCR6 in the function of these cells in the brain.
This research marks a significant advance in Alzheimer’s disease research, offering new insights into how the immune system interacts with the brain and pointing to potential targets for future treatments.
Understanding this complex relationship between the immune system and neurodegenerative diseases could be key to developing new therapeutic strategies.
If you care about Alzheimer’s, please read studies about Scientists find the root cause of Alzheimer’s disease and findings of Alzheimer’s might not be primarily a brain disease. A new theory suggests it’s an autoimmune condition.
For more information about Alzheimer’s disease, please see recent studies about Foods that reduce Alzheimer’s risk and results showing that Scientists link dietary antioxidants to Alzheimer’s prevention.
The research findings can be found in Nature Immunology.
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