Researchers have identified a link between immune activity around the brain and the emergence of dementia linked to high blood pressure. The findings were published in Nature Neuroscience.
The study focused on brain changes in mice with hypertension. Scientists observed unusually high levels of interleukin-17 (IL-17) in the cerebrospinal fluid of these animals. Further experiments showed that when IL-17 enters the brain, it activates macrophage cells, which heighten inflammation during infections. Mice engineered to be insensitive to IL-17 did not develop hypertension-related dementia, indicating that IL-17-driven activation of macrophages is a key driver of the cognitive decline observed in this model.
Researchers also pinpointed the source of IL-17 as immune cells residing in the brain’s protective membranes, the meninges. Normally, substances from the meninges stay out of the brain due to a selective barrier. In hypertension, this barrier appeared compromised, allowing IL-17 to reach brain tissue. An antibody that blocks IL-17 release was able to restore cognitive function in the mice, suggesting that therapies aimed at calming overactive meningeal immune cells could offer a new avenue for addressing hypertension-related dementia, according to the study.
Earlier studies have explored other angles, including the idea that antidepressants might influence neurodegenerative processes. While the current work centers on IL-17 and meningeal immunity, the broader landscape of dementia research continues to examine how immune signaling impacts brain health. The Nature Neuroscience report adds a distinct piece to this puzzle by linking meningeal IL-17 activity, macrophage activation, and cognitive decline in a hypertension context, and it underscores the potential of immune-targeted strategies to slow or prevent dementia associated with high blood pressure.
These findings come from a controlled set of experiments in animal models, which provide a platform for understanding how immune cells in and around the brain contribute to cognitive changes. If similar mechanisms are present in humans, therapies that limit IL-17 signaling or tamp down macrophage activation in the brain could become part of a broader approach to protecting brain function in people with hypertension. Future clinical studies will be needed to determine the safety and effectiveness of such strategies in people, and to evaluate how these immune pathways interact with other risk factors for dementia.
In summary, the study highlights a causal chain: hypertension can alter the brain’s protective barriers, allowing IL-17 from meningeal immune cells to trigger macrophage-driven inflammation, which in turn impairs mental performance. Blocking IL-17 shows promise in reversing these effects in mice, pointing toward potential new treatments that focus on the immune system to protect against hypertension-related cognitive decline, as reported by Nature Neuroscience.