Extracellular matrix signaling constitutively regulates cerebral blood flow in both physiological and pathological settings.

While Trypanosoma congolense is mostly known to cause a chronic wasting disease in animals, a new mouse model shows that acute cerebral trypanosomiasis is triggered by parasite sequestration and infiltration of T helper cells in the brain parenchyma.

Sex differences in the age-related decline of blood-brain barrier function vary across brain regions, with a more pronounced decrease observed in males beginning in the early 60s.

Cerebral subcortical microcirculation is more vulnerable to aging-induced changes and more responsive to exercise than cortical microcirculation.

An aorta smooth muscle-on-a-chip model indicated that NOTCH1 insufficiency in HAoSMCs induced phenotypic switching from a contractile to a synthetic phenotype accompanied by an impairment of mitochondrial fusion, implying its potential role as a therapeutic target for BAV-TAA.

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.

The number of inflows and outflows at the occluded capillary governs the local flow reduction, and the different topological configurations are probably designed for distinct functional tasks.

Mapping the fate of clogged brain capillaries reveals that VEGF signaling plays a critical role in dictating whether capillaries regain blood flow and persist or are pruned from the vascular tree.

The diameter of cortical arteries is not controlled by the overall neural activity, but rather by a subset of specialized neurons.

Modelling beta-amyloid deposition in bioengineered human vessels represents a notable advance to further investigate the role of the vasculature in Alzheimer's disease.