Fig. 5From: HMGB1 and thrombin mediate the blood-brain barrier dysfunction acting as biomarkers of neuroinflammation and progression to neurodegeneration in Alzheimer’s diseaseSchematic illustration of proinflammatory Aβ, DAMPs (HMGB1/S100B), and sRAGE acting at the BBB endothelium. Representation of BBB as source and target of neuroinflammation in AD. Endogenous damage molecules, DAMPs as well as Aβ, activate respective receptors to ramp up neuroinflammation. Soluble receptors such as sRAGE and sTM can neutralize some of these, and some may function as distinct biomarkers in progression of neurodegeneration in ADBack to article page