New antibody treatment blocks immune response to prevent Alzheimer's damage
Researchers at Washington University School of Medicine in St. Louis have identified a potential new approach to slowing Alzheimer’s-related brain damage by targeting the immune response rather than tau itself.
In mice with Alzheimer’s-like tau buildup, researchers used an antibody targeting CXCR3, a protein that helps T cells enter the brain. After several months of treatment, the mice had about half as many T cells in their brains, preserved roughly 40% more tissue in memory-related regions, and performed better on memory tests. Importantly, the treatment did not reduce tau levels, suggesting that limiting the immune response may help protect brain cells even when tau remains.
The findings build on earlier research showing that T cells accumulate in areas of the brain with high levels of tau and contribute to neurodegeneration. The researchers found that the chemokine CXCL10 and its receptor CXCR3 help guide these immune cells into the brain. Blocking either component prevented T-cell infiltration in the mouse models.
The study also found that the CXCR3 antibody did not need to enter the brain tissue to produce an effect. It acted at the brain’s borders, potentially offering an advantage because many treatments struggle to cross the blood-brain barrier.
Current Alzheimer’s drugs such as lecanemab and donanemab target amyloid and can slow disease progression, but they do not directly address primary tauopathies. The new findings suggest that targeting T-cell activity could represent a different therapeutic strategy for tau-related neurodegeneration.
The researchers emphasize that the approach has so far been tested only in mice and requires further research before it can be evaluated in people. Existing therapies that modify T-cell activity, including some treatments used for autoimmune and neurological disorders, could potentially provide avenues for future investigation.
