C-tau biomarker of neuronal damage in severe brain injured patients: association with elevated intracranial pressure and clinical outcome

Zemlan, Frank P.; Jauch, Edward C.; Mulchahey, J.J.; Gabbita, S. Prasad; Rosenberg, William S.; Speciale, Samuel G.; Zuccarello, Mario

doi:10.1016/s0006-8993(02)02920-7

Cited by 187 publications

(110 citation statements)

References 29 publications

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“…33 Consistent with this, the initial post-injury CSF levels of C-tau were found to be elevated in patients with severe TBI, correlated with clinical outcome (92% sensitivity; 94% specificity ), and predicted elevated ICP (78% sensitivity; 79% specificity). 37 …”

Section: Proteolytic Breakdown Productsmentioning

confidence: 99%

“…118 Elevated ICP can lead to further brain tissue damage via cerebral hypoperfusion, secondary ischemia, and brain tissue herniation, and may eventually result in death. 119 In a prospective study comparing the levels of C-tau between severe TBI and neurologic and non-neurologic controls, Zemlan et al 37 reported that serum C-tau levels could be used to differentiate those TBI patients with an ICP Ͻ30 mmHg from those with an ICP Ͼ30 mmHg. The serum levels of GFAP and S100B have also been proposed as markers capable of differentiating between TBI patients based on their ICP status.…”

Section: Intracranial Pressurementioning

confidence: 99%

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

et al. 2010

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Section: Proteolytic Breakdown Productsmentioning

confidence: 99%

Section: Intracranial Pressurementioning

confidence: 99%

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

et al. 2010

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“…MAP-tau is primarily a cytoskeletal protein which functions to stabilize microtubules. Upon CNS damage by a variety of insults, MAPtau appears to be proteolytically cleaved (Irazuzta et al, 2001, Zemlan et al, 2002. Cleaved tau (C-tau) concentrations have been shown to be increased following administration of the prototypic neurotoxins kainic acid and trimethyltin (Straiko et al, 2005 (submitted)) or following traumatic brain injury in rodents (Gabbita et al, 2005) and humans (Zemlan et al, 2002).…”

mentioning

confidence: 99%

“…Upon CNS damage by a variety of insults, MAPtau appears to be proteolytically cleaved (Irazuzta et al, 2001, Zemlan et al, 2002. Cleaved tau (C-tau) concentrations have been shown to be increased following administration of the prototypic neurotoxins kainic acid and trimethyltin (Straiko et al, 2005 (submitted)) or following traumatic brain injury in rodents (Gabbita et al, 2005) and humans (Zemlan et al, 2002). Notably, METH also has been reported to produce a time-dependent increase in C-tau in the striatum, hippocampus and, to a lesser extent, frontal cortex (Wallace et al, 2003).…”

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confidence: 99%

The effect of amphetamine analogs on cleaved microtubule-associated protein-tau formation in the rat brain

et al. 2007

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The present study quantified the cleaved form of the microtubule associated protein tau (cleaved MAP-tau, C-tau), a previously demonstrated marker of CNS toxicity, following the administration of monoamine-depleting regimens of the psychostimulant drugs amphetamine (AMPH), methamphetamine (METH), ±3,4-methylenedioxymethamphetamine (MDMA), or paramethoxyamphetamine (PMA) in an attempt to further characterize psychostimulant-induced toxicity. A dopamine (DA)-depleting regimen of AMPH produced an increase in C-tau immunoreactivity in the striatum, while a DA-and serotonin (5-HT)-depleting regimen of METH produced an increase in the number of C-tau immunoreactive cells in the striatum and CA2/CA3 and dentate gyrus regions of the hippocampus. MDMA and PMA, two psychostimulant drugs that produce selective 5-HT depletion in the striatum, had no effect on C-tau immunoreactivity in the striatum or hippocampus. Furthermore, 5,7-dihydroxytryptamine (5,7-DHT), an established 5-HT selective neurotoxin, did not produce an increase in C-tau immunoreactivity. Dual fluorescent immunocytochemistry with antibodies to GFAP and C-tau indicated that C-tau immunoreactivity was present in astrocytes, not neurons, suggesting that increased C-tau may be an alternative indicator of reactive gliosis. The present results are consistent with previous findings that the DA-depleting psychostimulants AMPH and METH produce reactive gliosis whereas the 5-HT-depleting drugs MDMA and PMA, as well as the known 5-HT selective neurotoxin 5,7-DHT, do not produce an appreciable glial response. Keywords methamphetamine; 3,4-methylenedioxymethamphetamine; amphetamine; paramethoxyamphetamine; 5,7-dihydroxytryptamine; toxicity Methamphetamine (METH) and ±3,4-methylenedioxymethamphetamine (MDMA) are substituted phenylethylamines whose popularity among young adults continues to be a public

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“…In the course of number of diseases, tau may be released from intracellular milieu and enter the brain parenchymal compartment and move continuously into the cerebrospinal fluid (CSF). Increased levels of tau have previously been described in CSF in the course of Alzheimer disease (AD) [8], Creutzfeldt-Jakob disease [9], meningoencephalitis [10], ischaemic stroke [11], and closed head trauma [12], whereas conflicting results can be found in respect to multiple sclerosis. Tau is regarded as a phosphoprotein, and phosphorylation is one of the main factors influencing both its physiological and pathological role [13].…”

Section: Introductionmentioning

confidence: 99%

CSF and serum total-tau and phospho-tau(181P) in MS patients

2011

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AbstractIn search of biological marker in multiple sclerosis (MS), total-tau and phospho-tau (Thr181) concentrations were established in CSF and serum of 78 patients with MS, using commercially available kits. Serum and CSF concentrations of IgG, IgM, and albumin were assayed simultaneously to calculate quotients and indices of intrathecal synthesis. Serum t-tau detection was strikingly low (23.1%); therefore, this factor was excluded from further analysis. Serum p-tau levels did not correlate with any of indices or quotients. Unexpectedly, CSF t-tau and p-tau showed an inverse relation with MSSS and EDSS, which has not been published elsewhere. Our results do not support utility of serum t-tau and p-tau as surrogate markers for MS.

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C-tau biomarker of neuronal damage in severe brain injured patients: association with elevated intracranial pressure and clinical outcome

Cited by 187 publications

References 29 publications

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

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

The effect of amphetamine analogs on cleaved microtubule-associated protein-tau formation in the rat brain

CSF and serum total-tau and phospho-tau(181P) in MS patients

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