Involvement of tau phosphorylation in traumatic brain injury patients

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Traumatic brain injury (TBI) is an increasing concern and serious health problem that is often caused by physical accidents such as falls, vehicle crashes, assault, and struck.1 After TBI, brain damage occurs rapidly, leading into a variety of symptoms including brain edema, concussion, even unconsciousness. In addition, long‐term deficits in cognitive, behavioral, or emotional functions can continue to affect patients after the injuries. As a result, the recovery from TBI is significantly impeded in approximately fifty per cent of patients with moderate or severe brain injures with poor outcomes.3 Nevertheless, the mechanisms underlying cognitive dysfunction due to TBI are still unclear, and consensus is lacking regarding the management of patients with TBI.4 Of particular, clinical importance for effective treatment to post‐traumatic brain injuries is therefore the thorough understanding of molecular changes responsible for cognitive impairment and neuropathological abnormalities.
Tau protein, a specific microtubule‐associated protein (MAP) in the central neural system, which can aggregate into intraneuronal filaments in neurodegenerative disorders,5 has emerged as a potential mediator of the neuron damage after TBI.7 Not only tau protein in both CSF (cerebrospinal fluid) and serum is elevated in brain trauma patients, but their levels are inversely correlated with the clinical improvement after the injuries. These changes can be observed soon after TBI and rapidly disappear after several days. The key properties of abnormal tau proteins in pathological conditions include hyperphosphorylation that may be related to an imbalance between the activities of phosphatases and kinases acting on tau in numerous neurological diseases.6 However, the potential involvement of abnormal tau phosphorylation has not been directly evaluated in the neuronal damages of TBI patients. Based on previous findings, we hypothesize that the rapid induction of tau phosphorylation could be detected at the focal site of injured brain tissues. Thus, we profiled the levels of total and phosphorylated tau protein in brain tissues harvested from patients with various severity of TBI. The investigations have also been involved with specific tau‐associated kinase GSK‐3β and phosphatase PP2A, to gain further mechanistic insights on the differential neurological responses to TBI.

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