The Neurovascular Interface

Evidence from in vitro experiments, animal models and humans is revisited and highlights the potential role of the blood-brain barrier in mediating the effects of non-invasive brain stimulation in AD.

Transcriptomics and proteomics studies show that the endothelial cell-specific genetic inactivation of Mer leads to pleiotropic deficits in angiogenesis, blood brain barrier formation, and blood coagulation.

Fiber-based speckle contrast optical spectroscopy measures human brain activation via cerebral blood flow changes, outperforming current methods.

A combination of optical imaging, electrophysiology, and BOLD fMRI in unanesthetized neonatal mice reveals that sleep-related vascular changes dominate over sensory-evoked changes.

Pharmacology and imaging of pericytes expressing GCaMP6f uncovers the basis of Ca2+ signaling in mid-capillary brain pericytes.

Human MRI data shows that parasagittal dura volume may not play a major role in cerebrospinal fluid clearance but could instead serve as a neuro-immune interface.

A multimodal approach is developed in rats, which enables the interrogation of effects of temperature changes on neurovascular coupling.

To understand if brain interstitial fluid/cerebrospinal fluid (ISF/CSF) exchange, CSF turnover, blood-brain barrier function or proteolysis were affected by aging or the presence of β amyloid plaques, Elbert et al. develop a non-steady state physiological model using MRI-derived brain volumes, stable isotope labeling kinetics of Aβ, and lumbar CSF Aβ concentration. Their model suggests an important role for blood-brain barrier transport and proteolytic degradation of Aβ in the development Alzheimer’s Disease in humans.

Smyth et al. use tissue microarrays from Alzheimer’s disease (AD) patient brains to show that PDGF-BB:PDGFRβ signalling components are reduced in AD. They then use primary human brain pericytes to elucidate a pathway by which PDGF-BB:PDGFRβ signalling in brain pericytes is disrupted in AD, thus impairing the blood brain barrier.

Multimodal imaging of the mouse brain following acute cocaine application revealed that cocaine caused a biphasic calcium response in neurons, but not astrocytes, suggesting that these cells play different roles in mediating neurovascular coupling to cocaine.