In mice, the high-salt diet reduced the resting cerebral blood flow by 28 per cent in the cortex and 25 per cent in the hippocampus brain regions involved in learning and memory. This impairment in the blood flow to the brain was caused by a decrease in the production of nitric oxide a gas generated by endothelial cells, the findings showed. “We discovered that mice fed a high-salt diet developed dementia even when blood pressure did not rise,” said Costantino Iadecola, Professor at the Weill Cornell Medicine in New York. “This was surprising since, in humans, the deleterious effects of salt on cognition were attributed to hypertension,” Iadecola added.
In the study, published in Nature Neuroscience, the mice were given food containing four per cent or eight per cent salt, representing an 8-to 16-fold increase compared to the high end of human salt consumption.Rodents that only ate the high-salt diet developed dementia and performed significantly worse on an object recognition test, a maze test and nest.
Further, as a result of the high salt intake, the mice’s white blood cells produced more interleukin 17 (IL-17) a protein is known to regulates immune and inflammatory responses and reduce nitric oxide in endothelial cells. However, when the researchers treated the mice with a drug called ROCK inhibitor Y27632, it reduced the levels of IL-17 and reduced the production of nitric oxide. The drug also improved the behavioural and cognitive functions in mice, Iadecola said.
“The IL-17-ROCK pathway is an exciting target for future research in the causes of cognitive impairment. It appears to counteract the cerebrovascular and cognitive effects of a high-salt diet,” explained Giuseppe Faraco, Assistant Professor at the varsity. The results illuminate a potential future target for countering harmful effects to the brain caused by excess salt consumption.