To prevent adverse health consequences, the World Health Organization recommends limiting salt intake to less than 5 grams per day
Posted Date – 12:52 AM, Tue – 5/30/23
To prevent adverse health consequences, the World Health Organization recommends limiting salt intake to less than 5 grams per day
Tokyo: Dementia is described as the loss of cognitive functions, including thinking, memory and reasoning, and is common in Japan. Currently, dementia treatment satisfaction is the lowest, and there is no drug treatment that can cure the disease. As the world’s population ages, it is critical to discover drugs to prevent and treat dementia.
Cognitive impairment has been linked to excessive consumption of table salt, a ubiquitous food seasoning. High salt (HS) intake can also lead to high blood pressure. To prevent adverse health consequences, the World Health Organization recommends limiting salt intake to less than 5 grams per day. Angiotensin II (Ang II), a hormone that plays a key role in regulating blood pressure and fluid homeostasis, and its receptor “AT1,” and the physiologically important lipid molecule prostaglandin E2 (PGE2, and its receptor) Involvement of ‘EP1’ in hypertension and neurotoxicity is well established. However, the role of these systems in HS-mediated hypertension and mood/cognitive impairment remains elusive.
To this end, a recent study published in the British Journal of Pharmacology thoroughly assessed various aspects of HS-mediated hypertension and emotional/cognitive impairment. The study was conducted by a team of collaborating researchers from Japan and shows how hypertension mediated by crosstalk between Ang II-AT1 and PGE2-EP1 leads to emotional and cognitive dysfunction.
Author Hisayoshi Kubota, of the Fujita Health University Graduate School of Health Sciences, commented: “Excessive salt intake is known to be a risk factor for hypertension, cognitive impairment, and dementia. However, focusing on the relationship between the peripheral and central nervous systems Interaction studies have not fully investigated this association.” According to published data, the addition of excess phosphate to the protein “tau” is largely responsible for this emotional and cognitive consequence. These findings are particularly noteworthy because tau is a key protein in Alzheimer’s disease.
The team first fed laboratory mice HS solution (2% NaCl in drinking water) for 12 weeks and monitored their blood pressure. “The effects of HS intake on mood/cognitive function and tau phosphorylation were also examined in two key regions of the mouse brain – the prefrontal cortex and the hippocampus,” explains Prof. Mouri. Next, they also investigated the role of Ang II-AT1 and PGE2-EP1 systems in HS-induced hypertension and neuronal/behavioral disturbances.
The results were remarkable and encouraging: several biochemical alternations occurred in the brains of the experimental mice. At the molecular level, in addition to adding phosphates to tau, the researchers observed a reduction in phosphate groups associated with a key enzyme called “CaMKII” — a protein involved in signaling in the brain. In addition, changes in the levels of “PSD95,” a protein that plays an important role in the organization and function of brain synapses (connections between brain cells), were also evident. Interestingly, the biochemical changes were reversed after taking the antihypertensive drug “losartan”. A similar reversal was observed after knockdown of the EP1 gene.
Collectively, these findings suggest that the angiotensin II-AT1 and prostaglandin E2-EP1 systems may be new therapeutic targets in hypertension-induced dementia.
