Cutting Down on Salt May Help Prevent Dementia

Dementia, a health issue that leads to loss of mental abilities like thinking, remembering, and reasoning, is very common in Japan. Right now, people are not too happy with the ways it’s being treated, and there’s no drug that can fully get rid of the disease. As the world’s population grows older, it’s crucial to find drugs that can stop or treat dementia.

Eating too much table salt, which is commonly used in our food, has been tied to problems in brain functions. Eating a lot of salt can also cause high blood pressure. To avoid these health issues, the World Health Organization suggests people should not have more than 5 g of salt per day. Certain body systems, including a hormone named angiotensin II (Ang II), its receptor “AT1”, and a key molecule prostaglandin E2 (PGE2 and its receptor “EP1”) known for its role in managing blood pressure and fluid balance, are known to be linked to high blood pressure and nerve damage. But, it’s not clear how these systems play a part in high blood pressure and brain problems caused by too much salt.

Recently, a study published in the British Journal of Pharmacology took a close look at these issues. The study, carried out by a group of researchers from Japan, found out how high blood pressure, caused by the interaction between Ang II-AT1 and PGE2-EP1, might lead to emotional and cognitive problems.

Author Hisayoshi Kubota from Fujita Health University’s Graduate School of Health Science says, “Excessive salt intake is considered a risk factor for hypertension, cognitive dysfunction, and dementia. However, studies focusing on the interaction between the peripheral and central nervous system have not sufficiently investigated this association.”

According to the data they gathered, the main cause of these emotional and cognitive problems is the addition of too many phosphates to a protein called “tau”. This is a key finding because tau is a major protein in Alzheimer’s disease.

The team started by giving lab mice a high-salt solution (2% NaCl in drinking water) for 12 weeks and tracked their blood pressure. “The effects of HS intake on emotional/cognitive function and tau phosphorylation were also examined in two key areas of the mouse brain—the prefrontal cortex and the hippocampus,” explains Prof. Mouri. After that, they also looked into the role of the Ang II-AT1 and PGE2-EP1 systems in high blood pressure and problems with the brain and behavior caused by high salt intake.

The results were quite promising: The mice’s brains had several changes. At the molecular level, other than adding phosphates to tau, they also saw a drop in the phosphate groups attached to a key enzyme called “CaMKII”, a protein that plays a part in brain signaling. There were also changes in the levels of “PSD95”, a protein that helps in the organization and function of brain synapses (the connection between brain cells). Interestingly, these changes went back to normal after giving the mice a high blood pressure drug called “losartan.” They noticed a similar effect after turning off the EP1 gene.

In the end, these findings suggest that angiotensin II-AT1 and prostaglandin E2-EP1 systems could be new therapeutic targets for dementia caused by high blood pressure.

Prof. Mouri sums up by saying, “This study is of particular social and economic importance because the annual social cost of dementia treatment in Japan is surging like never before”. That’s why it seems crucial for Japan’s fast-growing older population to find ways to prevent and treat dementia.

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