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HMGB1 and thrombin mediate the blood-brain barrier dysfunction acting as biomarkers of neuroinflammation and progression to neurodegeneration in Alzheimer's disease.

Barry W FestoffRavi K SajjaPatrick van DredenLuca Cucullo
Published in: Journal of neuroinflammation (2016)
Our current studies indicate that thrombin and HMGB1 are causal proximate proinflammatory mediators of BBB dysfunction, while sTM levels may indicate BBB endothelial damage; HMGB1 and sRAGE might serve as clinical biomarkers for progression and/or therapeutic efficacy along the AD spectrum.
Keyphrases
  • oxidative stress
  • blood brain barrier
  • traumatic brain injury
  • endothelial cells
  • lipopolysaccharide induced
  • lps induced
  • cognitive impairment
  • inflammatory response
  • brain injury
  • subarachnoid hemorrhage