The value of serum tau protein for the diagnosis of intracranial injury in minor head trauma

Kavalcı, Cemil; Pekdemir, Murat; Durukan, Polat; İlhan, Necip; Yıldız, Mustafa; Serhatlioğlu, Selami; Seçkin, Dilara

doi:10.1016/j.ajem.2006.10.008

Cited by 60 publications

(53 citation statements)

References 27 publications

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“…28,34 More recent publications using the more sensitive technology, Simoa, have demonstrated elevations of plasma tau after hypoxic-ischemic brain injury and sports concussion. 8,20 A recent study in boxers showed increased plasma tau immediately after a bout with head blows, but no loss of consciousness (LOC) followed by decrease in plasma tau to the prebout level after rest.…”

Section: Discussionmentioning

confidence: 99%

Increases of Plasma Levels of Glial Fibrillary Acidic Protein, Tau, and Amyloid β up to 90 Days after Traumatic Brain Injury

Bogoslovsky

Wilson

Yao

et al. 2017

Journal of Neurotrauma

165

126

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Glial fibrillary acidic protein (GFAP), microtubule-associated protein tau, and amyloid b peptide (Ab42) have been proposed as diagnostic and prognostic biomarkers in traumatic brain injury (TBI). Single molecule array (Simoa) is a novel technology that employs highly sensitive immunoassays for accurate measurements of candidate biomarkers found at low concentration in biological fluids. Our objective was to trace the trajectory of tau, GFAP, and Ab42 levels in plasma from the acute through subacute stages after TBI, compared with controls. Samples from 34 TBI subjects enrolled in the Citicoline Brain Injury Treatment Trial (COBRIT) were studied. Injury severity was assessed by Glasgow Coma Scale (GCS) and admission CT. Glasgow Outcome Scale Extended (GOSE) was assessed 6 months after injury. Plasma was collected within 24 h (Day 0), and 30 and 90 days after the TBI. Plasma collected from 69 healthy volunteers was used for comparison. At every time point, increases were noted in plasma GFAP ( p < 0.0001 for all comparisons), tau ( p < 0.0001, p < 0.0001, and p = 0.0044, at Days 0, 30, and 90, respectively), and Ab42 ( p < 0.001, p < 0.0001, and p = 0.0203, respectively) in TBI cases compared with controls. The levels were maximal at Day 0 for GFAP and tau and at Day 30 for Ab42. Area under curve (AUC) analyses for Day 0 GFAP and tau were excellent for discrimination of complicated mild TBI (cmTBI) from controls (0.936 and 0.901, correspondingly). Discriminant component analysis (DCA) for all three biomarkers at Days 0 and 30 differentiated controls from cmTBI (91.1% and 89.7% correctly classified, at each time point). Duration of post-traumatic amnesia (PTA) correlated weakly with tau levels at 30 days (Spearman's r = 0.40; 95% CI 0.0003-0.60, p = 0.044). The Marshall CT Grade on admission correlated weakly with Day 30 tau levels (Spearman's r = 0.41; 95% CI 0.04-0.68, p = 0.027). Day 30 Ab42 correlated with GOSE (standardized b -0.486, p = 0.042). GFAP, tau and Ab42 were increased up to 90 days after TBI compared with controls. Total tau levels correlated with clinical and radiological variables of TBI severity. Plasma Ab42 correlated with clinical outcome. Combination of all three biomarkers at Days 0 and 30 can be used to differentiate controls from cmTBI populations, and may be useful as biomarkers of TBI in both acute and subacute phases.

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Section: Discussionmentioning

confidence: 99%

Increases of Plasma Levels of Glial Fibrillary Acidic Protein, Tau, and Amyloid β up to 90 Days after Traumatic Brain Injury

Bogoslovsky

Wilson

Yao

et al. 2017

Journal of Neurotrauma

165

126

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“…101 One of the few other biomarkers that have been clinically tested in MTBI patients is tau. To test the diagnostic accuracy of C-tau in identifying MTBI patients with intracranial injuries, Kavalci et al 102 examined serum tau levels from 88 MTBI patients and correlated these changes with the presence or absence of intracranial lesions on their head CT. No significant difference in tau protein levels was detected between the two groups. In addition, no relationship has been found between initial serum C-tau levels and 3-month outcome.…”

Section: Biomarkers For Mild Tbimentioning

confidence: 99%

Biomarkers for the Diagnosis, Prognosis, and Evaluation of Treatment Efficacy for Traumatic Brain Injury

et al. 2010

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“…Increased tau levels have been reported in the CSF following TBI and also show promise as a specific serum biomarker in both human patients and experimental models. 13,15,16,[34][35][36] Although there is a rapid rise in tau protein levels in the CSF post-TBI, 13,34 the peak and temporal progression of serum tau levels have not been adequately evaluated. 15,16 Tau-associated neuropathology, particularly the presence of NFTs, has been reported in the brains of athletes who have played contact sports (boxers, football and ice hockey players, wrestlers) and who sustained concussions during their career.…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, establishing a complementary approach of patient evaluation using neurological assessment in combination with biochemical biomarkers will reliably and objectively determine the severity of a TBI, which can then guide treatment regimens. [11][12][13][14][15][16][17][18][19][20] Tau is a microtubule-associated protein localized mainly in neuronal cells and functions as a major structural element in the axonal cytoskeleton. Total tau (T-tau) is abundant in the central nervous system (CNS), and in particular, in unmyelinated axons and cortical interneurons.…”

Section: Introductionmentioning

confidence: 99%

A Novel, Ultrasensitive Assay for Tau: Potential for Assessing Traumatic Brain Injury in Tissues and Biofluids

Rubenstein

Chang

Davies

et al. 2015

Journal of Neurotrauma

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Traumatic brain injury (TBI) is a cause of death and disability and can lead to tauopathy-related dementia at an early age. Pathologically, TBI results in axonal injury that is coupled to tau hyperphosphorylation, leading to microtubule instability and tau-mediated neurodegeneration. This suggests that the forms of this protein might serve as neuroinjury-related biomarkers for diagnosis of injury severity and prognosis of the neurological damage prior to clinical expression. We initially determined whether we could detect tau in body fluids using a highly sensitive assay. We used a novel immunoassay, enhanced immunoassay using multi-arrayed fiberoptics (EIMAF) either alone or in combination with rolling circle amplification (a-EIMAF) for the detection of total (T) and phosphorylated (P) tau proteins from brains and biofluids (blood, CSF) of rodents following controlled cortical impact (CCI) and human patients post severe TBI (sTBI). This assay technology for tau is the most sensitive to date with a detection limit of approximately 100 ag/mL for either T-tau and Ptau. In the rodent models, T-tau and P-tau levels in brain and blood increased following CCI during the acute phase and remained high during the chronic phase (30 d). In human CSF samples, T-tau and P-tau increased during the sampling period (5-6 d). T-tau and P-tau in human serum rose during the acute phase and decreased during the chronic stage but was still detectable beyond six months post sTBI. Thus, EIMAF has the potential for assessing both the severity of the proximal injury and the prognosis using easily accessible samples.

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The value of serum tau protein for the diagnosis of intracranial injury in minor head trauma

Cited by 60 publications

References 27 publications

Increases of Plasma Levels of Glial Fibrillary Acidic Protein, Tau, and Amyloid β up to 90 Days after Traumatic Brain Injury

Increases of Plasma Levels of Glial Fibrillary Acidic Protein, Tau, and Amyloid β up to 90 Days after Traumatic Brain Injury

Biomarkers for the Diagnosis, Prognosis, and Evaluation of Treatment Efficacy for Traumatic Brain Injury

A Novel, Ultrasensitive Assay for Tau: Potential for Assessing Traumatic Brain Injury in Tissues and Biofluids

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