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Involvement of tau phosphorylation in traumatic brain injury patients
Author(s) -
Yang WJ.,
Chen W.,
Chen L.,
Guo YJ.,
Zeng JS.,
Li GY.,
Tong WS.
Publication year - 2017
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/ane.12644
Subject(s) - traumatic brain injury , hyperphosphorylation , glasgow coma scale , pathological , medicine , tau protein , phosphorylation , brain damage , central nervous system , tauopathy , neuroscience , psychology , alzheimer's disease , anesthesia , psychiatry , disease , neurodegeneration , biology , biochemistry
Objectives 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. Materials and 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 (R 2 =.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. Conclusion 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.