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Capillary stalling, micro-hypoxic pockets and micro-strokes : different sides of the same phenomena?
Exploiting advances in two-photon phosphorescence oxygen imaging in mice, our group recently showed that increasing age, atherosclerosis and Alzheimer’s disease (AD) are each associated with the emergence of increased capillary flow heterogeneity and sparse local micropockets of hypoxic tissue in the brain where neurons potentially die. In separate recent studies focusing on stroke and AD, vascular inflammation was shown to lead to the adhesion of neutrophils in capillaries, effectively blocking red blood cells (RBCs) passage, the oxygen carriers. What is not known is whether neutrophil adhesion and capillary RBC stalling cause hypoxic tissue micropockets and whether they persist over time to create tissue damage leading to cognitive impairments. The importance of the phenomenon was further underlined in the latter studies when an intervention blocking neutrophil adhesion was shown to improve memory (in AD mice) and motor recovery (in stroke mice). In this talk I will describe microscopic experiments, exploiting two- and three-photon microscopy and optical coherence tomography, that investigate the continuum from RBC transient stalls to micro-stroke and their impact on oxygenation.