A study published online in the British journal Nature on the 23rd confirmed the causal relationship between salt intake and cognitive function in mice. The study found that feeding mice a very high salt diet resulted in the accumulation of modified tau protein, which is related to diseases leading to dementia, such as Alzheimer's disease. Further research is needed to determine whether the results are applicable to humans.
Studies have shown that excessive salt intake is related to cognitive impairment and is a risk factor for dementia. Although the exact mechanism behind this association is unclear, vascular dysfunction and neuronal tau protein aggregation are considered to play a role in the development of cognitive impairment. This time, will & middot; Constantino & middot, a scientist at Cornell Medical College; Adkra and his colleagues found evidence of the latter effect and identified a signal cascade leading to the increase of phosphorylated tau protein.
They found that mice on a high salt diet, which contained 8 to 16 times as much salt as the diet of ordinary mice, decreased their ability to recognize new objects and their performance in Maze experiments. Studies have shown that high salt intake will reduce the synthesis of nitric oxide and activate an enzyme involved in tau protein phosphorylation: Cdk5. The recovery of nitric oxide synthesis can reverse the cognitive impairment in mice.
The researchers stressed that the high salt diet fed to mice actually exceeded the reported maximum human salt intake (3-5 times the recommended dose of 4g-5g per day). However, the findings identify a previously unknown link between eating habits and cognitive health, suggesting that avoiding a high salt diet may help maintain cognitive function.