Impact of High Dietary Salt on Neurovascular and Cognitive Functions

Dietary sodium intake in most world regions substantially exceeds physiological requirements, with well-documented consequences for cardiovascular and cerebrovascular health. Although the contribution of dietary salt to blood pressure elevation is well established, evidence from both experimental and human studies indicates that excess sodium adversely affects the cerebral vasculature and cognitive function through mechanisms that operate independently of blood pressure. Here, we review this evidence, integrating findings from animal models with observational and clinical data from human studies. Rodent studies consistently demonstrate that high-salt diet impairs cerebrovascular function and promotes cognitive decline, through mechanisms including IL (interleukin)-17A-mediated endothelial nitric oxide dysfunction, tau hyperphosphorylation, and neuroinflammation. In humans, growing evidence indicates that high dietary sodium accelerates cognitive decline and cerebral small vessel disease progression, though methodological limitations preclude definitive conclusions about causality in most studies. Critically, emerging evidence suggests that the relationship between dietary sodium and cognitive aging is nonlinear, with very low intake also associated with adverse outcomes. Taken together, the available evidence supports a role for dietary sodium in cerebrovascular and cognitive dysfunction that extends beyond its pressor effects, though adequately powered longitudinal studies combining gold-standard assessment of sodium intake with neuroimaging and cognitive end points are needed to establish causality with greater confidence.