Increase of neuron-specific enolase in patients with Creutzfeldt-Jakob disease

Kropp, Stefan; Zerr, Inga; Schulz‐Schaeffer, Walter; Riedemann, Christian; Bodemer, Monika; Laske, C; Kretzschmar, Hans A.; Poser, S.

doi:10.1016/s0304-3940(98)00992-6

Cited by 44 publications

(19 citation statements)

References 12 publications

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“…Indeed, reduced cNSE levels have been described in Alzheimer's disease (16). In contrast to other demential disorders, high cNSE levels have been described in Creutzfeldt-Jacob disease (17,18). It has been suggested that cNSE and CSF 14-3-3 protein may represent relevant information to establish the diagnosis of CreutzfeldtJacob disease.…”

Section: Introductionmentioning

confidence: 99%

Use of neuron-specific enolase for assessing the severity and outcome of neurological disorders in patients

Lima

Takayanagui

Garcia

et al. 2004

Braz J Med Biol Res

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Neuron-specific enolase (NSE) is a glycolytic enzyme present almost exclusively in neurons and neuroendocrine cells. NSE levels in cerebrospinal fluid (CSF) are assumed to be useful to estimate neuronal injury and clinical outcome of patients with serious clinical manifestations such as those observed in stroke, head injury, anoxic encephalopathy, encephalitis, brain metastasis, and status epilepticus. We compared levels of NSE in serum (sNSE) and in CSF (cNSE) among four groups: patients with meningitis (N = 11), patients with encephalic injuries associated with impairment of consciousness (ENC, N = 7), patients with neurocysticercosis (N = 25), and normal subjects (N = 8). Albumin was determined in serum and CSF samples, and the albumin quotient was used to estimate blood-brain barrier permeability. The Glasgow Coma Scale score was calculated at the time of lumbar puncture and the Glasgow Outcome Scale (GOS) score was calculated at the time of patient discharge or death. The ENC group had significantly higher cNSE (P = 0.01) and albumin quotient (P = 0.005), but not sNSE (P = 0.14), levels than the other groups (KruskalWallis test). Patients with lower GOS scores had higher cNSE levels (P = 0.035) than patients with favorable outcomes. Our findings indicate that sNSE is not sensitive enough to detect neuronal damage, but cNSE seems to be reliable for assessing patients with considerable neurological insult and cases with adverse outcome. However, one should be cautious about estimating the severity of neurological status as well as outcome based exclusively on cNSE in a single patient.

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Section: Introductionmentioning

confidence: 99%

Use of neuron-specific enolase for assessing the severity and outcome of neurological disorders in patients

Lima

Takayanagui

Garcia

et al. 2004

Braz J Med Biol Res

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“…The highly conserved nature of the 14-3-3 amino acid sequence makes the 14-3-3 test useful also in the ante mortem diagnosis of animals affected with transmissible spongiform encephalopathies [2] as well as in the diagnosis of cases of new variant CJD (vCJD) [3]. Other CSF protein markers which may be useful in distinguishing CJD from other neurological conditions are Tau [4], neuronspecific enolase (NSE) [5], S-100 [6] and amyloid beta 1-42 [7]. It has also been shown that apolipoprotein E (ApoE) levels in bovine spongiform encephalopathyaffected cattle appear to be higher than in control animals [8] although an initial study of ApoE CSF levels indicated no significant difference between patients with sporadic CJD (spCJD) and neurologic controls as measured with an ELISA assay [9].…”

Section: Introductionmentioning

confidence: 99%

Apolipoprotein E and other cerebrospinal fluid proteins differentiate ante mortem variant Creutzfeldt-Jakob disease from ante mortem sporadic Creutzfeldt-Jakob disease

et al. 2002

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The ability to perform an ante mortem differential diagnosis of Creutzfeld-Jakob disease (CJD) is aided by several clinical and molecular tests. There is a need for molecular tests which can reliably distinguish ante mortem variant CJD (vCJD) from ante mortem sporadic CJD (spCJD). A proteomics approach employing two-dimensional protein electrophoresis is applied to the study of ante mortem CSF samples obtained in collaboration with the CJD Surveillance Unit and the National Hospital for Neurology and Neurosurgery. The sample set includes two cases of vCJD, three cases of spCJD and three neurologic controls. Preliminary data using a panel of seven molecular markers is able to distinguish vCJD from spCJD using a heuristic clustering algorithm. One of the molecular markers has been identified as apolipoprotein E which appears to be upregulated in the cerebrospiral fluid (CSF) of patients with vCJD as compared to spCJD. Analysis of ante mortem CSF may help to differentiate patients with vCJD from those patients with spCJD.

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“…Otto et al [2] and Kropp et al [9] also demonstrated changes in NSE and S-100 in CSF at 2 points during the disease time course in 16 patients. Fifteen of these patients exhibited elevations in both markers which persisted until 30 weeks, although the levels decreased in 1 patient after 30 weeks.…”

Section: Discussionmentioning

confidence: 94%

“…A number of studies have reported changes in t-tau protein during 1 or 2 periods, but these studies have not analyzed the chronological progression [2,9,11] . t-tau protein levels peaked in Everbroeck's middle stage, corresponding to the clinical symptom of akinetic mutism.…”

Section: Discussionmentioning

confidence: 99%

Chronological Changes in MRI and CSF Biochemical Markers in Creutzfeldt-Jakob Disease Patients

Satoh

Shirabe

Eguchi

et al. 2007

Dement Geriatr Cogn Disord

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Background: There are currently no markers for evaluating chronological changes in Creutzfeldt-Jakob disease (CJD). We examined if chronological changes in biochemical markers in cerebrospinal fluid (CSF) and diffusion-weighted magnetic resonance imaging (DWI) were utilizable for this purpose. Methods: Ten independent patients were divided into two groups of 5 patients each. We analyzed CSF biochemical markers, DWI and the clinical course in one group. In the remaining group, only the CSF biochemical markers were analyzed before and after the onset of akinetic mutism. Results: The level of total tau (t-tau) protein in CSF in the early phase after disease onset was 2,655 ± 423.9 pg/ml, reaching a mean peak of 14,675 ± 1,240 pg/ml in the middle phase and gradually declining after that. Just before patients deteriorated into akinetic mutism, t-tau protein titers reached a maximum (8,786 ± 2,975 pg/ml). There were dramatic changes in t-tau protein levels throughout the clinical course, unlike the other markers. DWI was not always utilizable, because of discordance with clinical symptoms seen in this study. Four cases exhibited peaks in t-tau protein levels while the patients fell into akinetic mutism except 1 case. Conclusion: Our results suggest that t-tau protein is the most sensitive marker of disease progression in CJD patients.

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Increase of neuron-specific enolase in patients with Creutzfeldt-Jakob disease

Cited by 44 publications

References 12 publications

Use of neuron-specific enolase for assessing the severity and outcome of neurological disorders in patients

Use of neuron-specific enolase for assessing the severity and outcome of neurological disorders in patients

Apolipoprotein E and other cerebrospinal fluid proteins differentiate ante mortem variant Creutzfeldt-Jakob disease from ante mortem sporadic Creutzfeldt-Jakob disease

Chronological Changes in MRI and CSF Biochemical Markers in Creutzfeldt-Jakob Disease Patients

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