Study Reveals How High Salt Diet May Lead to Brain Inflammation - Video

A new study published in the journal Neuron reveals that a high-salt diet may cause brain inflammation, which in turn drives up blood pressure. Led by Masha Prager-Khoutorsky, associate professor in McGill University’s Department of Physiology, the research suggests that the brain—rather than just the kidneys—could be a key origin of hypertension.

Hypertension, or high blood pressure, affects about two-thirds of people over the age of 60 and is responsible for nearly 10 million deaths annually worldwide. Traditionally considered a disease of the kidneys and blood vessels, it is often asymptomatic but significantly increases the risk of heart attacks, strokes, and other serious health issues. However, up to one-third of patients fail to respond to standard medications—highlighting the need for a deeper understanding of alternative causes.

To simulate human eating patterns, researchers provided rats with water containing 2% salt—comparable to the sodium content in diets high in fast food, bacon, processed cheese, and instant noodles. This high-salt intake activated immune cells in a specific brain region, leading to inflammation and a spike in vasopressin, a hormone that raises blood pressure. The team used advanced brain imaging and modern laboratory techniques to observe these changes in real time.

“The brain’s role in hypertension has largely been overlooked, in part because it’s harder to study,” said Prager-Khoutorsky. “But with new techniques, we’re able to see these changes in action.”

The researchers opted to use rats rather than mice, as rats have salt and water regulation mechanisms that closely resemble those of humans, making the results more applicable.

The study offers crucial insight into the neurological basis of hypertension and could pave the way for brain-targeted therapies.

Reference: Gu, N., Makashova, O., Laporte, C., Chen, C. Q., Li, B., Chevillard, P. M., ... & Prager-Khoutorsky, M. (2025). Microglia regulate neuronal activity via structural remodeling of astrocytes. bioRxiv, 2025-02.