Martin Lauritzen

This study uses two-photon microscopy to reveal structural and dynamic features of the brain endothelial glycocalyx, including spatial heterogeneity, vesicular transport, and lectin-binding kinetics in vivo.

This study examines how brain precapillary sphincters regulate capillary blood flow in adult and aged mice during blood pressure surges, showing diminished myogenic response in older mice.

This study identifies vessel-type-specific vascular barrier dysfunction in Huntington's disease and shows partial rescue with an S1PR1 agonist.

The paper analyzes the BBB glycocalyx using multi-omic approaches, revealing unique glycan composition and structural features, and their potential role in neuroinflammation.

This study shows that neurovascular coupling in aged mice is slower and prolonged, with reduced Ca2+ signaling in vascular mural cells, and correlates with decreased spontaneous locomotion.

The paper uses two-photon microscopy to show that S1P signaling impairment causes glycocalyx loss in arterioles but not other vessel types in Apom-/- mice.

This study shows that astrocytic Ca2+ signals contribute to inhibitory neurovascular coupling in awake mice, with PVIN activity preceding NVC and depending on noradrenaline release.

This study identifies age-related impairments in brain microvascular dynamics, particularly in precapillary sphincters, leading to reduced neurovascular function in aging.

The paper investigates how nitric oxide, endothelin-1, and KATP channels modulate brain pericyte function, vascular tone, and neurovascular coupling through distinct signaling pathways.

The paper identifies post-capillary venules as the site for transcytosis of therapeutic nanoparticles across the blood-brain barrier.

This study shows that apoM-bound S1P regulates BBB permeability and transcytosis, with S1PR1 agonists able to restore permeability in apoM-deficient mice.

The paper investigates how cell-type-specific neuronal activity affects oxygen consumption and blood flow in mouse somatosensory cortex, finding that CMRO2 responses depend on neuronal excitation rather than induced gamma activity.

This study shows that somatosensory stimulation evokes astrocytic calcium signaling in the ischemic penumbra, with preserved responses in aged mice, suggesting astrocytic activity may contribute to neuroprotection after stroke.

This study identifies precapillary sphincters as regulators of cerebral blood flow, showing their dilation and constriction in response to neural activity and ischemia.