A study by the Faculty of Health Sciences of Fujita Health University (Japan) has shown a relationship between excessive salt intake and cognitive impairment and high blood pressure, which could be key to the development of preventive drugs and therapeutics against dementia.
Cognitive decline has previously been associated with excessive consumption of table salt. In addition, this habit can also cause hypertension. To avoid adverse health consequences, the World Health Organization (WHO) recommends limiting salt intake to less than 5 g per day.
The involvement of angiotensin II (Ang II) – a hormone that plays a key role in the regulation of blood pressure and fluid balance – and its ‘AT1’ receptor, as well as the physiologically important lipid molecule prostaglandin E2 (PGE2 and its ‘EP1’ receptor, in hypertension and neurotoxicity is I know well.
However, the involvement of these systems in salt-mediated hypertension and emotional/cognitive impairment remains elusive.
To this end, the aforementioned Japanese study, published in British Journal of Pharmacologythoroughly evaluated aspects of hypertension mediated high salt intake and emotional/cognitive disorders. Hypertension, mediated by crosstalk between Ang II-AT1 and PGE2-EP1, has been shown to cause emotional and cognitive dysfunction.
Author Hisayoshi Kubota reminds us that 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 systems have not sufficiently explored this connection,” he commented.
According to published data, the excessive addition of phosphates to the tau protein is primarily responsible for these emotional and cognitive consequences. The findings are particularly noteworthy because tau is a key protein in Alzheimer’s disease.
experiments on mice
For the study, the team first loaded laboratory mice with a high-salt solution (2% NaCl in drinking water) for 12 weeks and monitored their blood pressure.
“The effects of ingesting this amount of salt on emotional/cognitive function and tau phosphorylation in two key regions of the mouse brain were also examined.: prefrontal cortex and hippocampus,” explained Professor Akihiro Mouri. They then also studied the involvement of Ang II-AT1 and PGE2-EP1 systems in HS-induced hypertension and neuronal and behavioral damage.
According to the researchers, the results were “remarkable and encouraging” because the brains of the experimental mice showed various biochemical changes. At the molecular level, in addition to adding phosphates to tau, the researchers also observed a decrease in phosphate groups attached to a key enzyme called CaMKII, a protein involved in brain signaling.
Except, changes were also observed in the levels of PSD95, a protein that plays a critical role in the organization and function of brain synapses (connections between brain cells). The biochemical changes were reversed after administration of the antihypertensive drug losartan. A similar reversal was observed after knocking out the EP1 gene.
Taken together, these results suggest that the angiotensin II-AT1 and prostaglandin E2-EP1 systems could be novel therapeutic targets for hypertension-induced dementia.
Professor Mouri stressed that the study has “special social and economic significance” as the annual societal cost of treating dementia in Japan is rising “like never before”.
*With information from Europa Press.
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