How Salt Damages the Brain
New York – A high-salt diet may damage the brain in ways not previously suspected. Instead of an increase in blood pressure, animal experimental studies in
The high salt consumption in Western societies is one of the risk factors for cardiovascular diseases, which also include stroke and other circulatory disorders in the brain. For a long time, it was suspected that increased blood pressure, which results from a high-salt diet, is the main pathogenetic factor. However, the role of arterial hypertension is viewed critically, as restricting salt consumption does not lower blood pressure in all people, and this does not always result in a reduction in cardiovascular risk.
A team led by Costantino Iadecola from Weill Cornell Medical College in New York has now investigated the influence of a high-salt diet on mice. The supply of salt in the amount that roughly corresponds to the human diet in industrialized countries led to a decrease in blood flow in the brain after just a few weeks. The animals developed cognitive disorders: they sniffed objects that had been placed in their cages weeks before as intensively as if they were completely new to them.
The researchers were able to trace the circulatory disorders, which interestingly were not associated with an increase in blood pressure, back to endothelial dysfunction. The cells of the vascular wall lost the ability to produce nitric oxide (NO), which is normally used to widen the vessels when the brain needs more nutrients, for example during cognitive tasks.
The vascular function could be restored by administering L-arginine in the drinking water. L-arginine is a substrate for endothelial nitric oxide synthase (eNOS), which produces the gas nitric oxide, which widens the vessels and improves blood flow. Further investigations revealed that the high-salt diet disrupts the function of the enzyme eNOS. But why?
The researchers suspected the cause in the gut. Previous studies had shown that a high-salt diet increases the number of T helper cells that produce the cytokine interleukin (IL) 17. In fact, after administration of IL 17, the same changes occurred in cerebral blood flow and in the cognitive tests as after a high-salt diet. And an IL-17 antibody prevented a high-salt diet from causing a disturbance in cerebral blood flow.
IL 17 does not appear to directly disrupt the function of the enzyme eNOS. The point of attack appears to be a Rho-kinase (ROCK). The ROCK inhibitor Y27632 prevented IL 17 from disrupting blood flow in the brain by inhibiting eNOS.
The study provides several approaches as to how a negative influence of a high-salt diet on brain function could be prevented. This could be done through IL-17 antibodies, but also through a ROCK inhibitor. Whether new therapies will develop from this is difficult to predict. First of all, the conditions in mice cannot be transferred to humans (even if in vitro studies by the researchers suggest this). Then it is not certain that the active substances will prove to be tolerable and achieve the desired effect in clinical studies. The simplest way to avoid the negative effects on cerebral blood flow could be a lower-salt diet. © rme/aerzteblatt.de
Topics: