High levels of nervous system-specific proteins in cerebrospinal fluid in patients with early stage Creutzfeldt-Jakob disease

Jimi, Takahiro; Wakayama, Yoshihiro; Shibuya, Seiji; Nakata, Hiroumi; Tomaru, Teruaki; Takahashi, Yasutaka; Kosaka, Kenji; Asano, Taku; Kato, Kanefusa

doi:10.1016/0009-8981(92)90103-w

Cited by 82 publications

(52 citation statements)

References 17 publications

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“…8 Neuron-specific enolase (NSE) is a glycolytic enzyme that is localized primarily to the neuronal cytoplasm. In adults, CSF concentrations of NSE have served as markers of neuronal damage in patients with a variety of neurologic conditions including status epilepticus, 13 Creutzfeldt-Jakob disease, 14 and metastatic lung cancer. 15 NSE is also found in the CSF 16 -19 and serum 17 of adults after TBI.…”

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confidence: 99%

Neuron-Specific Enolase and S100B in Cerebrospinal Fluid After Severe Traumatic Brain Injury in Infants and Children

et al. 2002

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ABSTRACT. Background. Traumatic brain injury (TBI) is a leading cause of death and disability in children. Considerable insight into the mechanisms involved in secondary injury after TBI has resulted from analysis of ventricular cerebrospinal fluid (CSF) obtained in children with severe noninflicted and inflicted TBI (nTBI and iTBI, respectively). Neuron-specific enolase (NSE) is a glycolytic enzyme that is localized primarily to the neuronal cytoplasm. S100B is a calcium-binding protein localized to astroglial cells. In adults, CSF and serum concentrations of NSE and S100B have served as markers of neuronal damage after TBI. Neither NSE nor S100B has previously been studied in CSF after TBI in infants or children.Objective. To compare the time course and magnitude of neuronal and astroglial death after nTBI and iTBI by measuring CSF concentrations of NSE and S100B using a rapid enzyme-linked immunosorbent assay.Methods. Severe nTBI and iTBI were defined by strict clinical criteria. Serial ventricular CSF samples (n ‫؍‬ 35) were obtained from children 1.5 to 9 years with severe nTBI (n ‫؍‬ 5) and children 0.2 to 1.5 years (n ‫؍‬ 5) with severe iTBI. Lumbar CSF samples from 5 children 0.1 to 2.3 years evaluated for meningitis were used as a comparison group. CSF NSE and S100B concentrations were quantified by an enzyme-linked immunosorbent assay (SynX Pharma Inc, Ontario, Canada).Results. There was no difference in age between patients with iTBI (median [ ]). The initial Glasgow Coma Scale score was higher in the iTBI group (9 [4 -14]) versus the nTBI group (3 [3-7]). NSE was increased in TBI versus the comparison group in 34 of 35 samples. Mean NSE was markedly increased (mean ؎ SEM, 117.1 ؎ 12.0 ng/mL vs 3.5 ؎ 1.4 ng/mL). After nTBI, a transient peak in NSE was seen at a median of 11 hours after injury (range: 5-20 hours). After iTBI, an increase in admission NSE was followed by a sustained and delayed peak at a median of 63 hours after injury (range: 7-94). The magnitude of peak NSE was similar in nTBI and iTBI. S100B was increased versus the comparison group in 35 of 35 samples. Mean S100B was markedly increased in TBI versus the comparison group (1.67 ؎ 0.2 ng/mL vs 0.02 ؎ 0.0 ng/mL). S100B showed a single peak at 27 hours (range: 5-63 hours) after both nTBI and iTBI. The mean S100B concentration, peak S100B concentration, and the time to peak were not associated with mechanism of injury.Conclusions. Markers of neuronal and astroglial death are markedly increased in CSF after severe nTBI and iTBI. ITBI produces a unique time course of NSE, characterized by both an early and late peak, presumably representing 2 waves of neuronal death, the second of which may represent apoptosis. Delayed neuronal death may represent an important therapeutic target in iTBI. NSE and S100B may also be useful as markers to identify occult iTBI, help differentiate nTBI and iTBI, and assist in determining the time of injury in cases of iTBI. Pediatrics 2002;109(2). URL: http://www.pediatrics.org/ cgi/content/full/109/2/e31; head t...

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Neuron-Specific Enolase and S100B in Cerebrospinal Fluid After Severe Traumatic Brain Injury in Infants and Children

et al. 2002

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“…Kropp et al [9]demonstrated, in a longitudinal study, that the release of NSE was associated with disease progression. On the contrary, Jimi et al [10]described high levels of NSE, S-100b, creatine kinase and the alpha subunit of GT1-binding protein G0 during the early stages of the disease, but these markers returned to normal or were mildly elevated in the terminal phase. For 14-3-3 protein, the timing of appearance and changes in concentration are currently unknown.…”

Section: Discussionmentioning

confidence: 99%

Increased Detection of 14-3-3 Protein in Cerebrospinal Fluid in Sporadic Creutzfeldt-Jakob Disease during the Disease Course

Giraud¹,

Biacabe

Carrault³

et al. 2002

Eur Neurol

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Diagnosis of Creutzfeldt-Jakob Disease (CJD) is based on neurological signs associated with characteristic electroencephalographic activity or detection of 14-3-3 protein in cerebrospinal fluid. However, the time course of 14-3-3 protein release during sporadic CJD is unknown. We report two observations in which the level of the detected 14-3-3 protein increased significantly with time. These preliminary cases suggest that there may be an increased release of 14-3-3 protein during the course of CJD as already proven for iatrogenic CJD.

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“…For a biomarker to be useful, it should be easily obtainable from the cerebrospinal fluid, blood or urine and should identify children of all age groups with brain injury starting within the first few hours of life. Experimental studies done on primates have suggested that excessive neuroexcitation may result from activation of N-methyl- D -aspartate and muscarinic cholinergic receptors secondary to the release of glutamate and acetylcholine neurotransmitters [12]. The activation of N-methyl- D -aspartate receptors may lead to excessive calcium entry through these channels, which then leads to the activation of intracellular enzymes and a secondary activation of muscarinic receptors.…”

Section: Characterization Of An Ideal Biochemical Markermentioning

confidence: 99%

“…Svenmarker et al [31] also reported that 7 h after the end of coronary artery bypass, the S100B released from the fat cells is not detected in the blood, and increased S100B levels correlate with decreased memory function. Currently, one of the most accepted ways of applying the concept of S100B as a biomarker was developed by de Kruijk et al [32], who combined S100B levels with other predictors in order to increase the accuracy of predicting the clinical outcome in children with head injury [12,32]. …”

Section: Current Potential Markers In Mild Tbimentioning

confidence: 99%

Serum Biochemical Markers for Brain Damage in Children with Emphasis on Mild Head Injury

Menascu

Brezner²,

Tshechmer³

et al. 2010

Pediatr Neurosurg

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Despite the high incidence of mild pediatric head injuries, only within the past few years has there been increased interest and research in this area. This interest began when the findings from research done in adult patients showed that the effects of mild closed head injuries could interfere significantly with higher cognitive functioning, which impacted daily activities and employment. Traumatic brain injury (TBI) often involves a combination of mechanical trauma and local hypoxemia, on which serum biomarker concentrations may provide critical therapeutic data to time the brain injury. Biochemical serum markers after TBI may be used as a source for the identification of the injury, the extent of the injury and the time of its occurrence, and even for identifying its most likely outcome. This article discusses current research and theories regarding biochemical serum markers in brain injury with an emphasis on their impact on and utility in mild head injury in children.

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High levels of nervous system-specific proteins in cerebrospinal fluid in patients with early stage Creutzfeldt-Jakob disease

Cited by 82 publications

References 17 publications

Neuron-Specific Enolase and S100B in Cerebrospinal Fluid After Severe Traumatic Brain Injury in Infants and Children

Neuron-Specific Enolase and S100B in Cerebrospinal Fluid After Severe Traumatic Brain Injury in Infants and Children

Increased Detection of 14-3-3 Protein in Cerebrospinal Fluid in Sporadic Creutzfeldt-Jakob Disease during the Disease Course

Serum Biochemical Markers for Brain Damage in Children with Emphasis on Mild Head Injury

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