A study conducted by researchers at Washington University in St. Louis suggests that preventing certain immune cells from accumulating in the brain may slow neuronal damage associated with Alzheimer’s disease and similar conditions. The work builds on growing evidence that immune system activity plays a significant role in driving neurodegeneration, moving beyond previous focus on protein accumulation in the brain.
The research involved mice engineered to model Alzheimer’s disease and tauopathies, which are characterized by buildup of the tau protein. Scientists treated the animals with an antibody designed to block CXCR3, a molecule that immune cells use to navigate to sites of infection and tissue damage. This intervention prevented T cells from accumulating in the treated mice’s brains.
The results showed measurable improvements in the treated animals. Brain tissue loss in memory-related regions was 40% less in mice that received the antibody compared to untreated controls. Additionally, the treated mice performed better on standard memory tests than their untreated counterparts, even though both groups maintained similar levels of tau protein in their brains.
The findings, published in the journal Neuron, indicate a potential therapeutic approach that could reduce neurodegeneration without requiring medications that cross the blood-brain barrier, unlike current Alzheimer’s treatments. However, researchers acknowledged that it remains unclear whether the results observed in mice will translate to humans. Further investigation will be necessary to determine the clinical applicability of blocking this immune pathway in people with neurodegenerative diseases.
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