A recent study in Nature Neuroscience has made a significant discovery regarding the impact of chronic high blood pressure on cognitive decline, offering a new perspective on potential treatment strategies.
The study, led by Costantino Iadecola, M.D., of the Feil Family Brain and Mind Research Institute in New York City, used a mouse model to explore the relationship between hypertension (high blood pressure) and brain function.
The team’s findings suggest that immune system cells in the brain play a crucial role in the cognitive impairments associated with chronic high blood pressure.
Hypertension affects over a billion people globally and is known to lead to cognitive decline, sometimes even in the absence of a stroke.
However, previous attempts to mitigate cognitive loss in hypertensive patients without stroke have had mixed results. This new research brings fresh insights into the mechanisms at play.
The study focused on the response of immune cells within the brain’s protective covering, the meninges. The researchers found that in mice with hypertension, there was an abnormal activation of these immune cells, leading to impaired brain function.
Specifically, they observed increased levels of interleukin-17 (IL-17), a chemical that activates the immune system, in the cerebral spinal fluid and brain of these mice.
Interestingly, the study used a DOCA salt mouse model, which closely mimics low-renin hypertension, a common form of the condition in humans, particularly among Black Americans.
The model provided a realistic representation of human hypertension, making the findings more relevant.
Dr. Iadecola’s team also discovered that IL-17, once in the brain, activated macrophages – immune cells responsible for inflammation and infection response.
They confirmed the role of these macrophages in cognitive decline: mice with either a deletion of the IL-17 receptor in brain macrophages or depleted brain macrophages did not experience cognitive decline despite other symptoms of hypertension.
The source of IL-17 was another focus of the study. The team initially hypothesized that IL-17 came from the gut and traveled to the brain, damaging the brain blood vessels’ ability to respond to activity.
However, this only partially explained the cognitive impairment, suggesting another source of IL-17. They found that hypertension increased IL-17 production in the dura mater, one of the layers of the meninges.
Normally, barriers in the meninges prevent unwanted substances from entering the brain, but these barriers were disrupted in hypertensive mice, allowing IL-17 to spill into the cerebral spinal fluid.
Further experiments using a drug to prevent T-cell movement and an antibody to block T-cell activity in the meninges restored cognitive function in hypertensive mice. This suggests that targeting overactive T cells could be a novel treatment approach.
Dr. Iadecola’s findings are particularly important as they identify a new pathway through which hypertension may cause cognitive decline.
The study adds to previous research linking high salt diets to reduced nitric oxide production in brain vessels and subsequent tau protein build-up, a hallmark of Alzheimer’s disease.
The team is now investigating whether hypertension-induced suppression of nitric oxide also leads to increased tau production.
This research marks a significant step in understanding the complex relationships between hypertension, the immune system, and brain health.
It opens up new avenues for the treatment and prevention of cognitive impairments associated with high blood pressure.
If you care about blood pressure, please read studies about blood pressure drug that may increase risk of sudden cardiac arrest, and these teas could help reduce high blood pressure.
For more information about health, please see recent studies about nutrient that could strongly lower high blood pressure, and results showing this novel antioxidant may help reverse blood vessels aging by 20 years.
The research findings can be found in Nature Neuroscience.
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