A recent study by Japanese researchers highlights the detrimental impact of high salt intake on hypertension and its link to emotional and cognitive impairments. Specifically, the research reveals that the interaction between angiotensin II-AT1 and prostaglandin E2-EP1 systems is exacerbated by high salt consumption, leading to changes in tau protein and brain enzymes. These effects can contribute to dementia, a growing concern in Japan due to its aging population and the rising costs associated with dementia care. The study underscores the connection between high salt consumption, hypertension, and cognitive dysfunction, aiming to uncover new therapeutic targets for hypertension-induced dementia. The research involved subjecting mice to a high-salt solution for 12 weeks, monitoring their blood pressure, emotional, and cognitive functions. They found biochemical alterations linked to tau phosphorylation, which are characteristic of Alzheimer’s disease. Remarkably, these changes were reversed with antihypertensive treatment and genetic modification. This significant finding indicates that targeting the angiotensin II-AT1 and prostaglandin E2-EP1 pathways may hold promise for future dementia therapies. The urgency of developing effective treatments is accentuated by the increasing social costs of dementia care in Japan. The study was published in the British Journal of Pharmacology.
