Protecting brain cells from destruction remains one of the biggest challenges in treating Alzheimer's disease and related neurodegenerative conditions. These disorders, known as tauopathies, involve the buildup of abnormal tangles of a protein called tau inside the brain. As the tangles accumulate, nearby neurons begin to die.
However, growing evidence suggests that tau itself may not be responsible for most of the damage. Instead, the immune system's reaction to the protein appears to play a major role in the loss of brain cells, memory, and independence. Scientists at Washington University School of Medicine in St.
Louis have now identified a promising strategy for interrupting this damaging immune response. In mice with tau accumulation similar to that seen in Alzheimer's, researchers used an antibody to block a protein called CXCR3, which helps immune cells known as T cells enter the brain. After several months of treatment, the number of T cells inside the brain had fallen by approximately half.
The results were striking. Compared with untreated mice, animals receiving the antibody retained roughly 40% more tissue in brain regions involved in memory and performed better on a memory test. These improvements occurred even though the amount of accumulated tau remained unchanged.
The findings were published September 28 in the journal Neuron. "In tauopathies, including Alzheimer's disease, there's no treatment right now that actually decreases neurodegeneration," said David M. Holtzman, MD, senior author of the study and the Barbara Burton and Reuben M.
Morriss III Distinguished Professor in the Department of Neurology at WashU Medicine. "If we can show that we're really decreasing brain cell death, it's certainly worth trying to pursue that pathway to prevent the most devastating consequences of these diseases." Why Immune Cells May Be a Key to Alzheimer's Brain Damage Current Alzheimer's treatments primarily focus on removing amyloid, another protein associated with the disease. Two approved medications, lecanemab and donanemab, target amyloid plaques that develop between brain cells during the early stages of Alzheimer's.
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