Giuseppe Faraco

Neutrophil stalling does not mediate the increase in tau phosphorylation and the cognitive impairment associated with high salt diet

This study shows that capillary neutrophil stalling contributes to reduced cerebral blood flow in high salt diet but not to tau phosphorylation or cognitive impairment.

Hypertension-Induced Neurovascular and Cognitive Dysfunction at Single-Cell Resolution

This study uses scRNA-seq in a mouse hypertension model to identify early molecular changes in brain cells linked to neurovascular dysfunction and cognitive impairment.

Endothelial Sphingosine-1-Phosphate Receptor (S1PR) 1, a Functional S1PR in the Human Cerebrovascular Endothelium, Limits Blood Brain Barrier Permeability and Neuronal Injury following Subarachnoid Hemorrhage in Mice.

This study investigates the role of endothelial S1PR1 in maintaining BBB integrity and reducing neuronal injury after subarachnoid hemorrhage in mice and humans.

Molecular and functional alterations in the cerebral microvasculature in an optimized mouse model of sepsis-associated cognitive dysfunction.

This study develops and validates a mouse model of sepsis-induced cognitive dysfunction, identifying molecular and functional changes in the cerebral microvasculature and their association with cognitive impairment.

Meningeal IL-17 producing T cells mediate cognitive impairment in salt-sensitive hypertension

This study identifies meningeal IL-17-producing T cells as a key driver of cognitive impairment in hypertension, showing their role in activating brain macrophages and suggesting therapeutic targets.

Endothelial sphingosine-1-phosphate receptor 1 deficiency exacerbates brain injury and blood brain barrier dysfunction upon subarachnoid hemorrhage in mice.

This study shows that endothelial S1PR1 deficiency worsens brain injury and BBB dysfunction in mice after subarachnoid hemorrhage.

Dietary salt promotes cognitive impairment through tau phosphorylation

This study shows that a high-salt diet causes cognitive impairment in mice through tau hyperphosphorylation, which is prevented by restoring nitric oxide production.