A study published online Monday in the British journal nature confirms a causal relationship between salt intake and cognitive function in mice.
The study found that feeding the mice an extremely salty diet led to a buildup of a modified protein called tau, which in turn has been linked to conditions that lead to dementia, such as alzheimer's disease.
Further research is needed to determine whether the results apply to humans.
Excess salt consumption has been linked to cognitive impairment and is a risk factor for dementia.
Although the exact mechanism behind this association is unclear, both vascular dysfunction and tau accumulation in neurons are thought to play a role in the development of cognitive impairment.
This time, will Cornell medical college scientist clantino adkra and colleagues found evidence of the latter effect, identifying a signaling cascade that leads to an increase in phosphorylated tau.
They found that mice on a high-salt diet -- eight to 16 times as salty as the average mouse's diet -- were less able to recognize new objects and perform less well in the maze experiment.
Studies have shown that high salt intake reduces nitric oxide synthesis and activates an enzyme involved in tau phosphorylation: CDK5.
Restoring nitric oxide synthesis reversed cognitive impairment in mice.
The researchers note that the high-salt diet fed to the mice was in fact more than the maximum human salt intake ever reported (4g - 5g daily recommended three to five times).
However, the findings shed light on a previously unknown link between eating habits and cognitive health, suggesting that avoiding a high-salt diet may help maintain cognitive function.