Endothelium-Macrophage Crosstalk Mediates Blood-Brain Barrier Dysfunction in Hypertension.

Hypertension is a leading cause of stroke and dementia, effects attributed to disrupting delivery of blood flow to the brain. Hypertension also alters the blood-brain barrier (BBB), a critical component of brain health. Although endothelial cells are ultimately responsible for the BBB, the development and maintenance of the barrier properties depend on the interaction with other vascular-associated cells.

Publisher Correction: Dietary salt promotes cognitive impairment through tau phosphorylation.

An Amendment to this paper has been published and can be accessed via a link at the top of the paper.

Dietary salt promotes cognitive impairment through tau phosphorylation.

Dietary habits and vascular risk factors promote both Alzheimer's disease and cognitive impairment caused by vascular factors. Furthermore, accumulation of hyperphosphorylated tau, a microtubule-associated protein and a hallmark of Alzheimer's pathology, is also linked to vascular cognitive impairment. In mice, a salt-rich diet leads to cognitive dysfunction associated with a nitric oxide deficit in cerebral endothelial cells and cerebral hypoperfusion.

Dietary salt promotes neurovascular and cognitive dysfunction through a gut-initiated TH17 response.

A diet rich in salt is linked to an increased risk of cerebrovascular diseases and dementia, but it remains unclear how dietary salt harms the brain. We report that, in mice, excess dietary salt suppresses resting cerebral blood flow and endothelial function, leading to cognitive impairment. The effect depends on expansion of TH17 cells in the small intestine, resulting in a marked increase in plasma interleukin-17 (IL-17).