A causal link between salt intake and cognitive function in mice is identified in a study published online in Nature this week. The study uncovers how feeding mice an extremely high-salt diet can lead to the accumulation of modified tau — a protein associated with conditions that cause dementia, such as Alzheimer’s disease. Further research is needed to explore whether the results may be translated to humans.
Excessive salt consumption has been linked to cognitive impairment and is a risk factor for dementia. The precise mechanisms that underlie this association are unclear, but vascular dysfunction and the aggregation of tau proteins in neurons are thought to have a role in the development of cognitive impairment. Costantino Iadecola and colleagues find evidence for the latter, identifying a signalling cascade that culminates in increased levels of phosphorylated tau.
Mice that were fed a high-salt diet (8-16 times higher than a normal mouse diet) were less competent at recognizing new objects and struggled with a maze test. The authors show that high salt intake reduces nitric oxide synthesis, which leads to activation of an enzyme (CDK5) that is involved in tau phosphorylation. Cognitive impairment was reversed in mice by restoring nitric oxide production. The authors note that the high-salt diet fed to the mice exceeds the highest reported levels of salt consumption in humans (3-5 times the recommended level of 4-5 grams per day). Nevertheless, the results identify a previously unknown pathway linking dietary habits and cognitive health, which indicates that avoiding high-salt diets could maintain cognitive function.
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