Dementia is outlined because the lack of cognitive functioning-;together with considering, remembering, and reasoning-; and may be very prevalent in Japan. At present, the remedy satisfaction for dementia is among the many lowest and no drug remedy is out there to treatment the illness. With a quickly ageing world inhabitants, the event of dementia preventive and therapeutic medicine is vital.
Cognitive impairment has been linked to the consumption of extra desk salt, a ubiquitous meals seasoning. Excessive salt (HS) consumption can even result in hypertension. To forestall opposed well being outcomes, the World Well being Group recommends limiting salt consumption to lower than 5 g per day. The involvement of angiotensin II (Ang II)-;a hormone that performs a key position in regulating blood strain and fluid balance-; and its receptor “AT1”, in addition to that of the physiologically vital lipid molecule prostaglandin E2 (PGE2 and its receptor “EP1” in hypertension and neurotoxicity is well-recognized. Nonetheless, the involvement of those programs in HS-mediated hypertension and emotional/cognitive impairment stays elusive.
To this finish, a latest examine revealed within the British Journal of Pharmacology completely evaluated the features of HS-mediated hypertension and emotional/cognitive impairment. The examine was carried out by a group of collaborating researchers from Japan, and has proven how hypertension, mediated by the crosstalk between Ang II-AT1 and PGE2-EP1 causes emotional and cognitive dysfunction.
Writer Hisayoshi Kubota from Fujita Well being College’s Graduate Faculty of Well being Science feedback, “Extreme salt consumption is taken into account a threat issue for hypertension, cognitive dysfunction, and dementia. Nonetheless, research specializing in the interplay between the peripheral and central nervous system haven’t sufficiently investigated this affiliation.”
In accordance with the revealed knowledge, the addition of extreme phosphates to the protein “tau” is primarily answerable for this emotional and cognitive penalties. The findings are significantly noteworthy as a result of tau is a key protein of the Alzheimer’s illness.
The group first loaded laboratory mice with an HS answer (2% NaCl in ingesting water) for 12 weeks and monitored their blood strain. “The results of HS consumption on emotional/cognitive operate and tau phosphorylation have been additionally examined in two key areas of the mouse brain-;the prefrontal cortex and the hippocampus,” explains Prof. Mouri. Subsequent, additionally they studied the involvement of the Ang II-AT1 and PGE2-EP1 programs within the HS-induced hypertension and neuronal/behavioral impairment.
The outcomes have been outstanding and inspiring: The brains of the experimental mice had a number of biochemical alternations. On the molecular stage, in addition to the addition of phosphates to tau, the researchers additionally noticed a lower within the phosphate teams linked to a key enzyme known as “CaMKII”-;a protein concerned in mind signaling. Furthermore, modifications within the ranges of “PSD95”-;a protein that performs an important position within the group and performance of mind synapses (connection between mind cells)-;have been additionally evident. Curiously, the biochemical modifications have been reversed after the administration of the antihypertensive drug “losartan.” An identical reversal was noticed after knocking out the EP1 gene.
General, these findings counsel that angiotensin II-AT1 and prostaglandin E2-EP1 programs might be novel therapeutic targets for hypertension-induced dementia.
Prof. Mouri concludes by saying, “This examine is of specific social and financial significance as a result of the annual social value of dementia remedy in Japan is surging like by no means earlier than”. Due to this fact, creating preventive and therapeutic medicine for dementia appears vital for Japan’s quickly ageing inhabitants.“
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Journal reference:
Kubota, H., et al. (2023) Excessive salt induces cognitive impairment by way of the interplay of the angiotensin II-AT1 and prostaglandin E2-EP1 programs. British Journal of Pharmacology. doi.org/10.1111/bph.16093.
