NEW YORK / LONDON (IT BOLTWISE) – Scientists have identified a special group of microglia that have the potential to slow or prevent Alzheimer’s. This discovery could pave the way for new treatment strategies that target the brain’s immune cells.
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There is new hope in Alzheimer’s research: Scientists have discovered a special group of microglia that have the potential to positively influence the course of the disease. These microglia are characterized by low PU.1 levels and high expression of the receptor CD28, which leads to a reduction of inflammation in the brain.
Researchers at the Icahn School of Medicine at Mount Sinai and their international partners have found that these microglia not only suppress inflammation in the brain, but also slow the formation of amyloid plaques and the spread of toxic tau proteins. These two factors are crucial for the progression of Alzheimer’s disease.
PU.1 is a transcription factor that regulates gene expression, while CD28 acts as a signaling molecule on T cells and supports immune cell activation and communication. The researchers showed that removing CD28 from this group of microglia led to worsening inflammation and an increase in plaque formation, highlighting the importance of CD28 in the protective function of these cells.
This discovery could pave the way for new immunotherapeutic approaches to treat Alzheimer’s disease. The research was supported by various international organizations, including the National Institutes of Health and the European Research Council. The findings provide a new perspective on the role of microglia in Alzheimer’s disease and could lead to significant advances in treatment.
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