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Hypertension, Salt, and Dementia: New Insights into Brain Health and Therapeutic Approaches
A recent study from Japanese researchers, published in the British Journal of Pharmacology, has explored the effects of excessive salt intake on cognitive health, revealing important connections between hypertension and dementia. The researchers focused on the interaction between the angiotensin II-AT1 and prostaglandin E2-EP1 systems, which are amplified by high salt consumption. This interplay was found to induce hypertension, leading to emotional and cognitive impairments. Interestingly, these impairments were linked to changes in specific brain proteins, such as tau, a protein closely associated with Alzheimer’s disease. The researchers highlighted that these adverse effects could be reversed through antihypertensive medication or genetic modification, pointing to promising new therapeutic strategies for hypertension-induced dementia.
Dementia, characterized by cognitive decline in areas like memory, thinking, and reasoning, is increasingly common in Japan, largely due to its aging population. The study’s findings carry significant weight, as Japan, like many other countries, struggles with the escalating costs of dementia treatment. Currently, no curative treatment exists for dementia, which makes preventive measures critical. High salt consumption is already known to contribute to hypertension, and this research adds to a growing body of evidence suggesting that salt intake can directly impair cognitive and emotional functioning through its effects on the brain’s protein pathways.
The study used a mouse model, where subjects were given a high-salt (HS) solution for 12 weeks. The researchers monitored blood pressure and cognitive function, paying close attention to areas of the brain like the hippocampus and prefrontal cortex—regions essential for memory and decision-making. They identified a marked increase in tau phosphorylation, a process in which phosphate groups are added to the tau protein, disrupting its normal function and contributing to cognitive decline. Additionally, they observed a reduction in another critical brain protein, CaMKII, and altered levels of PSD95, a protein that plays a key role in synaptic function. These changes in brain biochemistry underscored the broader connection between high salt intake, hypertension, and brain health.
One of the most promising aspects of the study was the potential for reversing these negative effects. The researchers demonstrated that administering the antihypertensive drug losartan, which blocks the effects of angiotensin II, effectively restored cognitive function and normalized tau levels in the brain. Similarly, genetic knockout of the EP1 receptor—part of the prostaglandin E2 pathway—also reversed the harmful effects of high salt intake. These results not only deepen the understanding of how salt-induced hypertension affects the brain but also pave the way for new treatment approaches targeting specific pathways.
In conclusion, this study offers valuable insights into the biological mechanisms linking high salt consumption to cognitive impairment, suggesting that reducing salt intake and managing hypertension could be key strategies for preventing dementia. The researchers emphasize that these findings are especially significant in light of Japan’s aging society and the rising burden of dementia care. By identifying novel therapeutic targets in the angiotensin II-AT1 and prostaglandin E2-EP1 systems, this study opens the door for the development of more effective treatments for hypertension-related cognitive disorders, providing hope for mitigating the societal and economic costs of dementia.
