Salt: A Silent Killer

High salt intake causes cognitive impairment by activating angiotensin II-AT1 and prostaglandin E2-EP1 systems.

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Excessive salt consumption has long been associated with health concerns, particularly in relation to cognitive disorders and high blood pressure. This link between salt intake and these adverse conditions has prompted extensive research and sparked public health campaigns to raise awareness. 

Understanding the detrimental effects of excessive salt on cognitive function and cardiovascular health is crucial for individuals to make informed decisions about their dietary habits and take proactive measures to promote overall well-being. 

In this article, we delve into the compelling evidence behind the connection between excessive salt consumption, cognitive disorders, and high blood pressure, highlighting the importance of moderation in salt intake for a healthier lifestyle.

Dementia poses a significant challenge, particularly in Japan, where it is highly prevalent, and current treatment options are unsatisfactory. The aging global population further emphasizes the urgent need for preventive and therapeutic drugs for dementia. Recent research has highlighted a potential link between excessive salt consumption, cognitive impairment, and hypertension.

The World Health Organization recommends limiting daily salt intake to under 5 grams to prevent adverse health effects. While the involvement of angiotensin II and prostaglandin E2 in hypertension and neurotoxicity is known, their role in high salt-induced hypertension and emotional/cognitive impairment is not fully understood. 

A recent study published in the British Journal of Pharmacology by Japanese researchers has shed light on this relationship, demonstrating how the interaction between angiotensin II-AT1 and prostaglandin E2-EP1 contributes to hypertension and emotional/cognitive dysfunction.

These findings contribute to a better understanding of the impact of excessive salt consumption on cognitive health and provide potential avenues for future research and therapeutic interventions.

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

According to recent data, excessive phosphates added to the protein “tau” are primarily responsible for high salt intake’s emotional and cognitive consequences. This finding is significant as tau is a key protein in Alzheimer’s disease

In a study using laboratory mice, researchers observed the effects of high salt intake on blood pressure, emotional/cognitive function, and tau phosphorylation in the prefrontal cortex and hippocampus.

They also investigated the involvement of the angiotensin II-AT1 and prostaglandin E2-EP1 systems in hypertension and neuronal/behavioral impairment induced by high salt. 

The results revealed biochemical alterations in the mouse brains, including adding phosphates to tau, reduced phosphate groups in the CaMKII enzyme, and changes in PSD95 protein levels. Remarkably, these changes were reversed by administering the antihypertensive drug losartan and knocking out the EP1 gene. 

These findings suggest that targeting the angiotensin II-AT1 and prostaglandin E2-EP1 systems could be a promising approach for treating hypertension-induced dementia, which holds great significance for Japan’s aging population and the increasing social cost of dementia treatment.

In conclusion, high salt intake leads to cognitive impairment by interacting with the angiotensin II-AT1 and prostaglandin E2-EP1 systems. This interaction results in biochemical alterations in the brain, including adding phosphates to tau and changes in essential proteins involved in brain signaling and synaptic function. 

Understanding these mechanisms provides valuable insights into the link between excessive salt consumption and cognitive decline. Targeting the angiotensin II-AT1 and prostaglandin E2-EP1 systems may offer potential therapeutic approaches to mitigate hypertension-induced dementia.

Journal Reference:

  1. Kubota, H., Kunisawa, K., Wulaer, B.etal. High salt induces cognitive impairment via the interaction of the angiotensin II-AT1 and prostaglandin E2-EP1 systems. British Journal of Pharmacology. DOI: 10.1111/bph.16093
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