Costantino Iadecola

The paper uses ApHID-dextran to measure lysosomal pH in mouse meningeal phagocytes, revealing incomplete acidification and changes under pathological conditions.

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.

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.

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

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.

This paper develops a minimally invasive thrombotic stroke model in mice that allows for reperfusion therapy and in vivo imaging, showing it produces reproducible infarcts and is ameliorated by tPA.

The paper identifies ubiquitinated proteins in ischemic stroke using proteomics and shows that ubiquitination modulates kinase activity at the postsynaptic density.

The paper investigates the relationship between nNOS neuron activity and vascular responses in the barrel cortex of awake mice, finding distinct temporal roles for different nNOS neuron subsets in neurovascular coupling.

This study shows that inhibiting NOX2 reduces capillary stalling and inflammation in Alzheimer's mice, improving memory and blood flow.

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.

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

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

The paper uses AGO CLIP to identify miRNA-target interactions in the brain after ischemic stroke, revealing miR-29 family members lose target regulation, leading to rapid proteomic changes in glutamate homeostasis.

This study identifies neutrophil adhesion in brain capillaries as a cause of reduced cerebral blood flow and impaired memory in an Alzheimer's mouse model, showing that targeting this adhesion improves both CBF and memory.

This paper identifies a neuroprotective subpopulation of monocytes induced by lipopolysaccharide preconditioning that reduces brain injury after stroke in mice.