Tim Magnus

TL;DR: Results show that P2X7 receptors and pannexin-1 channels are major mediators of postanoxic depolarization in neurons and of brain damage after ischemia, and that they operate in the same deleterious signaling cascade leading to neuronal and tissue demise.

TL;DR: This research was supported by the Intramural Research Program of the NIH, National Institute on Aging and the authors have no conflicts of scientific interest with respect to the manuscript.

TL;DR: The role of neuroinflammation in ischemic stroke pathology is critically discussed, focusing on the BBB and the interactions between central nervous system and peripheral immune responses, and the possibility of clinical implementation of imaging modalities to assess stroke-associated neuro inflammation with the potential to provide image-guided diagnosis and treatment.

TL;DR: In vivo, transient middle cerebral artery occlusion and reperfusion in kinase-dead PI3Kδ or wild-type mice pre- or post-treated with the PI3kδ inhibitor CAL-101, leads to reduced TNF levels, decreased leukocyte infiltration, reduced infarct size and improved functional outcome.

TL;DR: It is demonstrated that therapeutic approaches targeting synergistic IL-17 and tumor necrosis factor-&agr; pathways in parallel offer additional neuroprotection in stroke, and brain-infiltrating IL-18–positive T cells belong to the subset of natural IL- 17–producing T cells.