Analysis of a mouse model of megalencephalic leukoencephalopathy with subcortical cysts (MLC) shows that the astrocyte-specific membrane protein MLC1 sustains the postnatal development of perivascular astrocytic processes and that MLC is a developmental disorder of the gliovascular unit.

Excitatory and inhibitory cortical neurons drive parallel vasodilatory pathways, while vasoconstriction is mediated exclusively by inhibition acting via Neuropeptide Y binding to Y1 receptors.

Mice modelling atherosclerosis show neurovascular breakdown in the cortex compared to healthy controls, and inducing atherosclerosis in mice modelling Alzheimer's disease increases the number of amyloid plaques in the hippocampus.

Local tissue hypoxia follows seizures, is responsible for postictal behavioural dysfunction rather than the seizures per se and can be treated.

Understanding how loss of CO₂/H⁺ vascular reactivity affects respiratory control may facilitate development of treatments for breathing problems in this population.

Reactive endothelial venules are a new vessel subtype characterized by consistent expression of cell adhesion molecules, preferential leukocyte transmigration, association with perivascular macrophages, and the initiation of CNS immune responses.

Neural stem cells in the dentate gyrus have unique cytoplasmic processes that promote privileged access to circulating factors by a unique contact point with an endothelial cell.

Sleep-related hemodynamic signals are much larger than those in the awake brain, so it is crucial to monitor the arousal state during studies of spontaneous activity.

Analyses based on the mouse model of a human genetic disease reveal that the neuron production of cerebral tissue can be boosted by escalated signaling between neural progenitors and the vasculature.

Increases of extracellular potassium silence capillary pericyte calcium signaling, suggesting a participation of capillary pericytes in the potassium-mediated neurovascular communication.