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PubMed1990

[Diagnostic value of biochemical tumor markers in brain tumors. Review of the literature and own experience with serum analysis of sialic acid (NANA), carcinoembryonic antigen (CEA) and neuron-specific enolase (NSE)].

In a review of the literature the current knowledge of the diagnostic significance of sialic acid (NANA), neuron-specific enolase (NSE) and carcinoembryonic antigen (CEA) in the detection and differentiation of brain tumors is demonstrated. The efficiency of some additional biochemical tumor markers is briefly described. In a total of 101 patients of our own 63 patients operated on intracranial expansive lesions and 38 patients with non-tumoral diseases of the central nervous system were examined for their serum concentrations of NANA, NSE and CEA with additional determination of total serum protein (TSP) and C-reactive protein (CRP) concentrations. 24 benign, 15 semibenign, 12 semimalign and 12 malign expansions were compared with each other and with the controls for their tumor marker concentrations. The criteria of the diagnostic reliability (sensitivity, specificity, positive and negative predictive value) were calculated for each single marker and the reliability of information for the combined used markers was evaluated. In summary the following results were found: The concentration of C-reactive protein corresponded significantly with the NANA-concentrations on the one hand and with the CEA-concentrations on the other hand (p less than 0.05). NANA: 1. The average concentration increased with increasing malignancy (no significance). 2. Patients who suffered from non-tumorous diseases of the central nervous system which coincided with brain tissue lesions had often extremely high values. 3. 4 of 10 healthy controls had NANA-levels above the reference value. 4. The sensitivity was 44%, the specificity 73%, the positive predictive value 17%, the negative predictive value 88% (patients with pathological CRP- or TSP-values excluded).(ABSTRACT TRUNCATED AT 250 WORDS)

Biomarkers, Tumor↗
PubMed1987

[Serum NSE (neuron-specific enolase) levels in small cell lung cancer, with special reference to the measurement of serial serum NSE levels].

Serum neuron-specific enolase (NSE) was measured in 105 patients with lung cancer without prior therapy. Increasing serum levels of NSE were observed in 84% of cases of small cell lung cancer (SCLC). 11% of adenocarcinomas, 18.5% of squamous cell carcinomas and 37.5% of large cell carcinomas. Serum NSE levels changed in parallel with the effect of initial treatment. Although two of 5 patients with SCLC, in whom serial NSE levels were measured after treatment, showed elevation of serum NSE levels before clinical relapse, elevated serum NSE levels were not observed in 3 patients at clinical relapse. These data seem to suggest that measurement of serial NSE is useful for predicting relapse prior to clinical recognition. However, it still remains an important point to carry out clinical general surveillance for relapse.

Adult↗
PubMed1985

[Neuron-specific serum enolase in patients with non-tumor pathologies].

In this brief communication, the authors indicate that amounts of neuron-specific enolase higher than 30 ng/ml are observed only in 1% of non-tumoral processes, and that when found in patients with respiratory symptoms a microcytic carcinoma of the lung can be suspected in 97% of the cases.

Adult↗
PubMed1994

Prognostic value of cerebrospinal fluid neuron-specific enolase and S-100b protein in Guillain-Barré syndrome.

We measured the cerebrospinal fluid (CSF) concentrations of neuron-specific enolase (NSE) and S-100b protein (S-100b) using enzyme immunoassay methods, in 24 patients with Guillain-Barré syndrome and 46 controls, and examined their prognostic values. Sixteen of 24 patients showed elevated levels (> the mean + 2SD levels of controls) of NSE, S-100b, or both, and in those with higher NSE or S-100b levels there was a rather longer duration of disease, whereas 8 patients with the normal levels showed an early recovery. Further, NSE or S-100b levels were significantly correlated with months to recovery. Thus, NSE and S-100b in CSF may be useful markers for predicting the outcome of Guillain-Barré syndrome.

Adolescent↗
PubMed2003

Human synapsin 1 gene promoter confers highly neuron-specific long-term transgene expression from an adenoviral vector in the adult rat brain depending on the transduced area.

Targeting therapeutic transgene expression to defined tissues is a major task in the development of safe and efficient gene therapy protocols. Recombinant adenovirus is an attractive vector because it can be prepared in huge quantity and new generation vectors possess very large cloning capacities combined with reduced immunogenicity. In the brain, adenovirus transduces mainly glial cells, making it difficult to use this vector system in applications that need expression of therapeutic proteins in neurons. Here, we show that by using a small fragment of the human synapsin 1 gene promoter, we were able to restrict transgene expression from an adenoviral vector exclusively to neurons. Furthermore, we obtained stable long-term transgene expression from this vector in striatum and thalamus at appropriate vector dose. Other promoters like the CMV and U1snRNA promoters also mediated transgene expression over several months, but mainly in glial cells. Although the NSE promoter was relatively neuron specific, it still expressed in glial cells also, and was clearly outperformed by the synapsin promoter with respect to transcriptional neuronal targeting. As an important feature of adenoviral-mediated gene transfer to the brain, we demonstrate that dopaminergic neurons of the substantia nigra do not allow for long-term expression from adenoviral vectors. Strikingly, these neurons appeared to specifically attenuate transgene expression by deleting the adenoviral genome.

Adenoviridae↗
PubMed1996

Neuron-specific enolase as an aid to outcome prediction in head injury.

A statistically significant elevation was observed in serum and CSF neuron-specific enolase (NSE) levels in patients with major head injury, relative to control individuals. No correlation was noted between serum NSE and either APACHE II, Injury Severity Score (ISS), Glasgow Outcome Score (GOS) or Glasgow Coma Scale (GCS). A significant correlation was noted between CSF NSE levels and GCS, but not between CSF NSE and APACHE II, ISS or GOS. Of the patients with major head injury, 100% had NSE CSF levels above the normal level, while 47% had elevated serum NSE levels. In nine patients with major head injury, changes in CSF levels reflected changes in serum NSE levels. In all nine patients, serum NSE decreased to reach normal values, regardless of the outcome as predicted by the GOS. Therefore, while NSE would appear to be a marker of neuronal cell damage, other markers are also essential.

Adult↗
PubMed2006

Increased lipid peroxidation and neuron specific enolase in treatment refractory schizophrenics.

It is well-known that increased lipid peroxidation and failure of antioxidant mechanisms leads to neuronal damage in schizophrenic patients. However, this neurodegenerative mechanism has not been studied in treatment refractory schizophrenics (TRS). Therefore, the main purpose of this study was to determine neuronal damage in TRS in comparison to non-refractory schizophrenics (NRS) by means of quantitative analysis of lipid peroxidation and neuron specific enolase (NSE) related to the psychopathology severity. Two groups of paranoid schizophrenics, TRS and NRS, and a group of healthy controls (CO) were assembled (n=13). Lipid peroxidation was analyzed through spectrophotometry for quantification of malonaldehyde (MDA) and 4-hydroxynonenal (4-HNE) serum concentrations. As well, serum NSE was quantified by radioimmunoassay (ELSA). Psychopathology was evaluated using the brief psychiatric rating scale (BPRS) and the positive and negative symptoms scale (PANSS). TRS showed significant higher concentrations of lipoperoxides by-products and NSE, than NRS and CO. Clinical scores also revealed a more severe pathology in TRS, than in NRS. Raised lipoperoxidation correlated with higher delusions and emotional withdrawal symptoms, and increased NSE correlated with a lower flow of the conversation and lack of spontaneity. All these results together suggest that TRS patients suffer a greater lipid peroxidation and neuronal damage than NRS, apparently related to worsening of some of the psychiatric symptoms.

Adult↗
PubMed1994

Four structurally distinct neuron-specific olfactomedin-related glycoproteins produced by differential promoter utilization and alternative mRNA splicing from a single gene.

Four structurally related neuron-specific 1B426b mRNAs, designated AMY, BMY, AMZ, and BMZ, have been isolated from rat brain cDNA libraries. The four mRNAs are related to one another by their shared M region and by two pairs of alternative 5' (A, B) or 3' (Y, Z) regions. All four possible combinations were detected. The four transcripts are derived by differential promoter utilization (to generate A or B 5' ends) and alternative splicing (to generate Y or Z 3' ends) of the primary transcripts of the single D2Sutle gene. All four mRNAs were detected in most brain regions, but were enriched within the cortex and hippocampus. In the pituitary only the two A-type and in the adrenal glands only the two B-type mRNAs were detected. In situ hybridization shows a highly heterogeneous distribution across brain regions, paralleling the Northern blot results and additionally identifying the reactive cells as neurons. The cDNAs encode related glycoproteins of 125, 153, 457, and 485 amino acids, which have been detected immunochemically. The AMZ and BMZ proteins show significant sequence similarity with olfactomedin, an extracellular matrix protein of bullfrog olfactory epithelium, suggesting the possibility of a matrix-related function for these rat glycoproteins in neurons and neurosecretory cells.

Animals↗
PubMed1991

I-POU: a POU-domain protein that inhibits neuron-specific gene activation.

A novel, structurally distinct POU-domain protein has been identified that inhibits activation by another positive POU-domain regulator of neuron-specific transcription units. Two Drosophila POU-domain proteins, I-POU and Cf1-a, are coexpressed in overlapping subsets of neurons during development. Because I-POU lacks two basic residues in the N terminus of its homeodomain, it cannot bind DNA, but it does form a stable heterodimeric complex with Cf1-a, preventing Cf1-a from binding to DNA recognition elements and from transactivating the dopa-decarboxylase gene. The inhibition by I-POU provides a potential strategy by which the activation of genes in development is controlled by a homeodomain-containing protein that does not bind DNA.

Amino Acid Sequence↗
PubMed2000

GM1 enhances the association of neuron-specific MAP2 with actin in MAP2-transfected 3T3 cells.

The ganglioside GM1 is a glycosphingolipid which enhances process formation of several neuronal lines and potentiates some growth factor-mediated responses. Previously we have shown that 24 h exposure of Neuro 2a cells to GM1 mobilized the neuron-specific microtubule-associated protein, MAP2, away from microtubule-rich areas to areas of neurite sprouting where MAP2 was more closely associated with the subcortical actin network. To examine the role of GM1 in fostering the shift of the association of MAP2 from tubulin to actin, NIH 3T3 cells were co-transfected with pHook-1, which expresses a surface antigen, and a construct expressing MAP2. Transfected cells were selected with magnetic beads coated with a hapten that binds to the expressed surface antigen and treated with 150 microg/ml GM1 for 18-24 h. Actin and MAP2 or tubulin and MAP2 were immunolocalized and examined with confocal microscopy. MAP2 was found throughout the cytoplasm as well as associated with actin filaments. As observed previously with Neuro 2a, GM1 treatment of transfected fibroblasts redistributed the MAP2 away from direct association with microtubules to peripheral areas where the association of MAP2 with actin was enhanced. GM1 did not induce neurite-like processes in MAP2-transfected cells. Treatment with cytochalasin B, which is reported to result in process formation, also did not induce neurite-like processes. These studies suggest that GM1's ability to mobilize MAP2 and promote its association with actin is not restricted to neurons.

3T3 Cells↗
PubMed1996

The onconeural antigen Nova-1 is a neuron-specific RNA-binding protein, the activity of which is inhibited by paraneoplastic antibodies.

Nova-1, a protein expressed in tumors and neurons, is a target antigen in a human paraneoplastic motor disorder [paraneoplastic opsoclonus-myoclonus ataxia (POMA)]. We evaluated the relationship between the function of Nova-1 and its role as a disease antigen. We show that Nova-1 is a neuron-specific RNA-binding protein with sequence and functional similarities to FMR-1. Nova-1 mRNA is restricted to the subcortical nervous system, and the protein binds to RNA with high affinity. Nova-1 KH domains mediate this RNA binding, and point mutations within them abrogate binding. POMA disease antisera (6/6) recognize the third KH domain but not an inactive point mutant, and affinity-purified antibody blocks Nova-1 RNA binding. Thus, a cardinal feature of POMA is the production of antibodies that inhibit Nova-1-RNA interactions, suggesting such inhibition may cause the neurological disease.

Amino Acid Sequence↗
PubMed2003

Serum neuron-specific enolase and S-100B protein in cardiac arrest patients treated with hypothermia.

BACKGROUND AND PURPOSE: High serum levels of neuron-specific enolase (NSE) and S-100B protein are known to be associated with ischemic brain injury and poor outcome after cardiac arrest. Therapeutic hypothermia has been shown to improve neurological outcome after cardiac arrest. The aim of this study was to evaluate the effect of therapeutic hypothermia on levels of serum NSE and S-100B protein, their time course, and their prognostic value in predicting unfavorable outcome after out-of-hospital cardiac arrest. METHODS: Seventy patients resuscitated from ventricular fibrillation were randomly assigned to hypothermia of 33+/-1 degrees C for 24 hours or to normothermia. Serum NSE and S-100B were sampled at 24, 36, and 48 hours after cardiac arrest. Neurological outcome was dichotomized into good or poor at 6 months after cardiac arrest. RESULTS: The levels of NSE (P=0.007 by analysis of variance for repeated measurements) but not S-100B were lower in hypothermia- than normothermia-treated patients. A decrease in NSE values between 24 and 48 hours was observed in 30 of 34 patients (88%) in the hypothermia group and in 16 of 32 patients (50%) in the normothermia group (P<0.001). The decrease in NSE values was associated with good outcome at 6 months after cardiac arrest (P=0.005), recovery of consciousness (P<0.001), and survival for at least 6 months after cardiac arrest (P=0.012). CONCLUSIONS: Decreasing levels of serum NSE but not S-100B over time may indicate selective attenuation of delayed neuronal death by therapeutic hypothermia in victims of cardiac arrest.

Adolescent↗
PubMed2004

Retrograde regulation in the CNS; neuron-specific interpretations of TGF-beta signaling.

Retrograde signals influence neuronal survival, differentiation, synaptogenesis, and plasticity. Several recent papers describe novel roles for the well-studied TGF-beta pathway in retrograde synaptic signaling. While each dissects spatial and molecular aspects of TGF-beta signaling in a specific synaptic context, together these studies demonstrate that a specific retrograde signal may be interpreted in diverse, neuron-specific ways. Thus, a neuron's intrinsic properties and its other extrinsic signaling inputs determine its cellular and genomic response to TGF-beta.

Animals↗
PubMed1983

Raised neuron-specific enolase in serum of children with metastatic neuroblastoma. A report from the Children's Cancer Study Group.

Serum levels of neuron-specific enolase (NSE) were measured by radioimmunoassay at diagnosis in 122 children with widespread metastatic neuroblastoma (clinical stage IV). 96% of these patients had NSE levels more than three standard deviations above the mean for age-matched normal children. Mean serum NSE was 207 +/- SD257 ng/ml (range 10-1240 ng/ml), whereas that in normal age-matched children was 7.5 +/- 2.1 ng/ml (range 5.4-12.9 ng/ml). Analysis of survival in relation to the level of NSE at diagnosis suggested that serum levels greater than 100 ng/ml were associated with a poor outcome. This relation was highly significant in the subgroup of infants less than 1 year old at diagnosis; all 7 with serum NSE below 100 ng/ml were alive up to 36 months after diagnosis, whereas 7 of 8 with serum NSE above 100 ng/ml died within 12 months of diagnosis. Serum NSE may be a useful disease marker and a prognostic indicator in children with metastatic neuroblastoma.

Child↗
PubMed1987

Neuron-specific enolase (NSE) as a tumour marker and comparative evaluation with carcinoembryonic antigen (CEA) in small-cell lung cancer.

Serum neuron-specific enolase (NSE) was evaluated in a number of malignant tumours. It was elevated (greater than 12.5 micrograms l-1) in 13/17 (76.5%) patients with extensive small-cell lung carcinoma and in none of the three patients with limited disease. Of patients with carcinoma of the breast 4/12 (33.3%) had elevated concentrations. Normal concentrations were found in patients with non-Hodgkin's lymphoma (19) and Hodgkin's disease (15), carcinoma of the cervix (2), CSF and serum (5) of patients with gestational trophoblastic disease (with definite nervous system involvement). Comparative serial studies of NSE and carcinoembryonic antigen (CEA) concentrations were done in 15 patients with small-cell lung cancer (SCLC). Of these 7/15 (46.7%) had elevated pre-treatment concentrations of both CEA and NSE, 1/15 (6.7%) had CEA elevated only, while 2/15 (13.3%) had NSE alone elevated. Of those patients with normal pre-treatment marker concentrations 3/5 (60%) had elevated markers on recurrence. The mean survival period was 61.9 weeks; 66.8 weeks for the marker-negative group and 44.6 weeks for the marker-positive (both NSE and CEA) group. Combined NSE and CEA evaluation provide additional means of monitoring SCLC.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1999

Total synthesis of a cholinergic neuron-specific ganglioside GT1a alpha: a high affinity ligand for myelin-associated glycoprotein (MAG).

An efficient total synthesis of a cholinergic neuron-specific ganglioside GT1a alpha (IV3NeuAcIII6NeuAcII3NeuAc-GgOse4Cer) is described. The suitably protected sialyl-alpha(2-->6)-gangliotriose (III6NeuAc-GgOse3) derivative was glycosylated with the phenyl 2-thioglycoside of sialic acid in the presence of N-iodosuccinimide (NIS) and trimethylsilyl trifluoromethane-sulfonate (TMSOTf) in acetonitrile medium, giving the disialogangliotriose (III6NeuAcII3NeuAc-GgOse3) derivative which contains both sialyl-alpha(2-->6)-GalNAc and sialyl-alpha(2-->3)-Gal structures (Route I). This pentasaccharide was efficiently synthesized also by the coupling of (methyl 5-acetamido-4,7,8,9-tetra-O-acetyl-3,5-dideoxy-D-glycero-alpha-D-galacto -2-nonulopyranosylonate)-(2-->6)-2-deoxy-3,4-O-isopropylidene-2-ph thalimido-D-galactopyranosyl trichloroacetimidate with 2-(trimethylsilyl)ethyl (methyl 5-acetamido-4,7,8,9-tetra-O-acetyl-3,5-dideoxy-D-glycero-alpha-D-galacto -2-nonulopyranosylonate)-(2-->3)-(2,6-di-O-benzyl-beta-D-galactopy ranosyl)-(1-->4)-2,3,6-tri-O-benzyl-beta-D-glucopyranoside, followed by conversion of the phthalimido group to the acetamido group (Route II). O-Deisopropylidenation and further glycosylation with methyl (methyl 5-acetamido-4,7,8,9-tetra-O-acetyl-3,5-dideoxy-D-glycero-alpha-D-gala ct-2-nonulopyranosylonate)-(2-->3)-2,4,6-tri-O-benzoyl-1-thio-b eta-D-galactopyranoside, promoted by dimethyl(methylthio)sulfonium triflate (DMTST), gave the desired trisialogangliotetraose (IV3NeuAcIII6NeuAcII3NeuAc-GgOse4) derivative, which was converted stepwise into the title ganglioside GT1a alpha by the introduction of the ceramide part and then complete deprotection. The ganglioside obtained was shown to be identical with the native GT1a alpha on TLC-immunostaining.

Animals↗
PubMedDate not supplied

Immunohistochemical staining of granular cell tumour for neurone specific enolase: evidence in support of a neural origin.

Eight cases of benign granular cell tumour of tongue and skin all showed immunohistochemical staining for neurone specific enolase (NSE). Four Schwannomas, two neurofibromas and Schwann cells of nerves related to these tumours and the granular cell tumours showed no staining for NSE. NSE is a marker for neuronal type cells of the nervous system and cells of the neuroendocrine system. The results support a neural derivation of granular cell tumours. The histogenetic precursor may be an undifferentiated spindle-shaped 'reserve' cell of peripheral nerve, perhaps necessary for replacement of shed sensory organs.

Cytoplasmic Granules↗
PubMed1990

Identification of injury-induced mitotic cells in adult rat cerebral cortex by neuron-specific markers.

Adult rat brains were injured by partial decortication. Four days later, the brains were examined for mitotic cells that were immunostained for neuronal markers: the neuron-specific enolase (NSE) and neurofilaments (NF). Of the 30 rats stained for NSE, 15 were found to have NSE-positive cells containing mitotic figures; of the 25 rats stained for NF, 12 possessed NF-positive cells in mitosis. Most of the mitotic neurons were granule cells and small- and medium-size pyramidal cells and were located in cortical layer III within 500 microns from the wound margin. Although a rare phenomenon, mitosis of neurons in the neocortex of mature mammalian brains may reflect neuronal plasticity in response to injury.

Animals↗