title: Involvement of tau phosphorylation in traumatic brain injury patients.
abstract: OBJECTIVE
  Traumatic brain injury (TBI) results in significant morbidity and mortality throughout the world. In TBI patients suffering cognitive, emotional, and behavioral deficits, the leading cause derives from the physical injury to the central nervous system (CNS) that impairs brain function.
  
  
  METHODS
  Here, we applied a targeted approach to understand the potential mechanisms of neuron damage after TBI. Tau protein phosphorylation was compared in the brain tissues collected from patients underwent brain surgery based on the assessment of brain injury extent by Glasgow Coma Scale (GCS).
  
  
  RESULTS
  The results indicated that the levels of phosphorylated tau were significantly higher in the severe and extremely severe TBI groups, compared to the moderate group of patients. Phosphorylated, but not the total tau protein was uniquely correlated with the GCS score (R2=.7849, P<.01) in 142 TBI patients. Consistently, the activities of key players associated with tau hyperphosphorylation GSK-3β and PP2A showed parallel correlations with the severity of TBI as well.
  
  
  CONCLUSIONS
  These data suggest that the enhanced tau protein phosphorylation occurs upon severe neuron injures and may contribute to the pathological structural changes of CNS leading to brain damage of TBI.
authors.affiliation: Department of Neurosurgery, The People's Hospital of Pudong New Area, Shanghai, China.
authors.forename: W-J
authors.initials: WJ
authors.lastname: Yang
authors.affiliation: Department of Neurosurgery, The People's Hospital of Pudong New Area, Shanghai, China.
authors.forename: W
authors.initials: W
authors.lastname: Chen
authors.affiliation: Department of Neurosurgery, The People's Hospital of Pudong New Area, Shanghai, China.
authors.forename: L
authors.initials: L
authors.lastname: Chen
authors.affiliation: Department of Neurosurgery, The People's Hospital of Pudong New Area, Shanghai, China.
authors.forename: Y-J
authors.initials: YJ
authors.lastname: Guo
authors.affiliation: Department of Neurosurgery, The People's Hospital of Pudong New Area, Shanghai, China.
authors.forename: J-S
authors.initials: JS
authors.lastname: Zeng
authors.affiliation: Department of Neurosurgery, The People's Hospital of Pudong New Area, Shanghai, China.
authors.forename: G-Y
authors.initials: GY
authors.lastname: Li
authors.affiliation: Department of Neurosurgery, The People's Hospital of Pudong New Area, Shanghai, China.
authors.forename: W-S
authors.initials: WS
authors.lastname: Tong
mesh_terms: D000328:Adult; D000070642:Brain Injuries, Traumatic / Q000378:metabolism* / Q000473:pathology; D005260:Female; D015600:Glasgow Coma Scale; D000071679:Glycogen Synthase Kinase 3 beta / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D010766:Phosphorylation; D054648:Protein Phosphatase 2 / Q000378:metabolism; D011499:Protein Processing, Post-Translational; D016875:tau Proteins / Q000378:metabolism*
chemical_list: D016875:tau Proteins; D000071679:Glycogen Synthase Kinase 3 beta; D054648:Protein Phosphatase 2
keywords: GSK-3β; PP2A; cognitive impairment; tau phosphorylation; traumatic brain injury