Researchers have identified a unique type of immune cell in the brain that actively works to slow the progression of Alzheimer’s disease. This groundbreaking discovery, published in the journal Nature, reveals how certain microglia reduce inflammation. They also block the spread of harmful proteins.
These specialised cells offer a promising new direction for developing effective therapies against neurodegenerative diseases.
The international research team found that microglia with low levels of a protein called PU.1 and high levels of a receptor known as CD28 possess protective qualities. These specific cells work to suppress widespread brain inflammation. They also slow the accumulation of amyloid plaques and toxic tau proteins.
Recent studies show new antibody drugs can slow cognitive decline in people with early-onset Alzheimer’s — a critical finding for a disease with no cure.
CBS News chief medical correspondent @DrLaPook visits Washington University School of Medicine in St. Louis, where… pic.twitter.com/pExhhpzU56
— CBS Sunday Morning 🌞 (@CBSSunday) November 9, 2025Senior author Professor Anne Schaefer emphasized the significance of the finding. “Microglia are not simply destructive responders in Alzheimer’s disease,” she stated. “They can become the brain’s protectors.”
This research provides a clear explanation for earlier genetic studies. Previous work had linked a common genetic variant in the SPI1 gene, which produces PU.1, to a lower risk of developing Alzheimer’s.
For the first time, a study suggests that Alzheimer's disease may be preventable if treatment begins early, before symptoms appear. CBS News' @DrLaPook spoke with the doctor leading the clinical trial. pic.twitter.com/cUcu08Bi1Q
— CBS Evening News (@CBSEveningNews) November 8, 2025“These results provide a mechanistic explanation for why lower PU.1 levels are linked to reduced Alzheimer’s disease risk,” said senior co-author Dr. Alison Goate.
The discovery of the PU.1-CD28 pathway strengthens the case for immune-based treatments. It suggests that future therapies could be designed to boost the activity of these protective microglia. This could potentially alter the course of the disease.
