Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P10636 (tau protein)
 5,110 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two clonal immortalized neurons designated SN6.1b and SN6.2a were isolated by limiting dilution from a mouse embryonic septal cholinergic neuronal hybrid cell line SN6 (Hammond et al., 1986). In the serum-containing medium without extra differentiating agents, one-third of SN6.1b cells stably exhibited a morphology of differentiated neurons with extensive elaborate neurites, while a majority of SN6.2a cells, along with the parent cell line SN6, were round in shape with poorly branched short processes. Neurochemical studies showed that both clones synthesized choline acetyltransferase (ChAT), dopamine, norepinephrine, serotonin, and glutamate. Immunocytochemically, they expressed a number of neuronal antigens, such as 200-kDa neurofilament protein, neuron-specific enolase, microtubule-associated protein 2, tau protein, tubulin, neural cell adhesion molecule, Thy-1.2, saxitoxin-binding sodium channel protein, ChAT, tyrosine hydroxylase, serotonin, and glutamate. The coexistence of cholinergic, catecholaminergic, serotonergic, and glutamatergic neurotransmitter markers in the clonal hybrid septal neurons that express a variety of immunocytochemical properties of differentiated neurons suggests that embryonic septal cholinergic neurons are potentially multiphenotypic with respect to neurotransmitter synthesis.
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PMID:Coexistence of cholinergic, catecholaminergic, serotonergic, and glutamatergic neurotransmitter markers in mouse clonal hybrid neurons derived from the septal region. 135 85

Two clonal immortalized neurons designated CL8c4.7 and CL8a5.2 were established by somatic cell fusion between a hypoxanthine phosphoribosyltransferase-(HPRT-) deficient neuroblastoma N18TG2 and newborn mouse cerebellar/brain stem neurons. In the serum-containing medium without extra differentiating agents, both clones exhibited a morphology of differentiated neurons. They contained high levels of glutamate but no gamma-aminobutyric acid (GABA). The CL8a5.2 clone synthesized choline acetyltransferase and serotonin. In immunocytochemical studies, both clones expressed 200 kD neurofilament protein, neuron-specific enolase, microtubule-associated protein 2 (MAP2), tau protein, neuronal cell adhesion molecule (N-CAM), HNK-1, Thy-1.2, saxitoxin-binding sodium channel protein, and glutamate. Synaptophysin immunoreactivity was identified in the neuritic terminals of CL8c4.7 cells. Most of these antigens were barely detectable on N18TG2 cells. Electrophysiologically, both clones generated action potentials in response to electrical stimuli. The hybrid clones that express characteristics of differentiated neurons derived from the cerebellar and brain stem regions might be invaluable for the study of the molecular basis of neuronal differentiation and degeneration in these regions.
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PMID:Establishment of mouse-immortalized hybrid clones expressing characteristics of differentiated neurons derived from the cerebellar and brain stem regions. 135 6

Newborn rat nasal tissues containing olfactory epithelium were dissociated and maintained in a monolayer cell culture. Neurons were present, as determined by immunostaining with antibodies to 4 neuron-specific proteins: neuron-specific enolase, microtubule-associated protein 2, tau protein and synaptophysin. Immunostained neurons had a distinctive morphology resembling olfactory neurons. By patch-clamp analysis, these cells were electrically active. Responses of some neurons to physiological concentrations of an odorant mixture identified them as olfactory receptor cells.
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PMID:Cultured rat olfactory neurons are excitable and respond to odors. 235 Aug 78

Evidence from retroviral marking techniques and immortalized cell lines indicates that multipotential stem cells exist in many areas of the developing central nervous system. However, the factors that influence the commitment of these stem cells into distinct neuronal or glial lineages are not known. We have created an immortalized hypothalamic cell line derived from embryonic day 14 hypothalamic cells with a replication-defective retroviral construct containing a temperature-sensitive allele (tsA58) of the large T antigen of the simian virus 40. The clonality of this cell line, which we have named V1, was established by single cell cloning and by Southern blot analysis. V1 cells exhibit two different morphologies: the vast majority of cells are flat and stellate, and a smaller number are phase-bright round cells with processes. V1 cells express nestin and neural-cell adhesion molecule, typical of proliferating neuroepithelial cells. They also express glial fibrillary acidic protein and S100 as well as the low molecular weight neurofilament protein. In addition, the phase-bright, process-bearing V1 cells stain intensely for many typical neuronal proteins, such as low, medium and high molecular weight neurofilament proteins, tau protein, microtubule-associated protein-2, and neuron-specific enolase. The phase-bright cells also have condensed chromatin and display mitotic spindles, indicating that they are in mitosis. When V1 cells are transferred from the permissive temperature (33 degrees C) to the restrictive temperature (39 degrees C), there is a decrease in expression of NF-L and an increase in expression of NF-H and glial fibrillary acidic protein in the flat V1 cells. The enhanced expression of neuronal antigens in mitotically active V1 cells is novel and may represent a more general property of the differentiation process. We suggest that V1 cells arise from a mixed neural/glial neuroepithelial progenitor cell that expresses both neuronal- and glial-specific proteins in the developing hypothalamus.
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PMID:An immortalized mouse neuroepithelial cell line with neuronal and glial phenotypes. 882 20

There is a need for improvement of the diagnosis of vascular dementia (VaD). Today, the clinician has to rely on clinical examination, history, and, possibly, brain imaging to identify cerebrovascular damage and other signs of VaD. The clinical diagnosis of subcortical VaD may be difficult because the clinical manifestation of this disorder is often similar to that of Alzheimer disease. There are also mixed forms of the two disorders. Biochemical diagnostic markers, which reflect the pathogenetic processes in the brain, would add to the accuracy of the diagnosis. There are some interesting candidate markers: the cerebrospinal fluid (CSF)/serum albumin ratio could be used to identify blood-brain barrier damage to the small intracerebral vessels, CSF sulfatide to identify ongoing demyelination of the white matter, CSF neuron-specific enolase to identify ongoing neuronal degeneration, and CSF tau protein and CSF neurofilament light protein to identify ongoing axonal degeneration. None of these potential markers is specific to subcortical VaD, but together and used in conjunction with the conventional diagnostic workup, they may be of diagnostic value.
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PMID:Cerebrospinal fluid markers of pathogenetic processes in vascular dementia, with special reference to the subcortical subtype. 1060 88

Despite a significant reduction in the frequency of lumbar taps done for CSF examination this method is still an important diagnostic tool. In recent years important advances have been made in the studies of the cytology and biochemistry of CSF. The introduction of new simple methods of centrifugation has increased the index of cell recovery with better possibilities of differentiation of these cells. In the biochemistry of proteins in which the analysis of immunoglobulins, albumins and other proteins, such as 14-3-3 protein, S-100, tau protein, enzymes, such as neuron-specific enolase or matrix-metalproteinase, alkaline myelin protein, beta-2-microglobulin, various cytokines, has been introduced, it is becoming a routine analysis in many CSF laboratories. The role of determination of many antibodies is increasing. Particular advances have been achieved in genetic studies, and, similarly as in other medical disciplines, explanation is expected of many not yet sufficiently clear pathological mechanisms.
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PMID:[Present condition and prospects of cerebrospinal fluid diagnostics]. 1173 69

A 53-year-old-woman presenting with pelvic discomfort was found to have a 9.5 cm tumor located in the wall of the ileon. Light microscopy showed that the tumor was made of fascicles of plump spindle cells and bizarre epithelioid cells. A cuff of lymphoid cells was also present at the tumor margin. The tumor cells strongly expressed tau protein, neuron-specific enolase, protein green product 9.5 and glial fibrillary acid protein (GFAP), but did not show positive immunostaining for S-100 protein, CD34 or CD117. The tumor showed unequivocal ultrastructural evidence of neural differentiation. Skeinoid fibers were scattered throughout the tumor. This is the first mixed neuronal-glial tumor of the digestive tract to be described in the literature. Such histological and immunohistochemical features could be misinterpreted as features of digestive schwannoma. We suggest that this tumor is distinct from gastrointestinal stromal tumors in lacking CD34 and CD117 expression.
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PMID:Mixed neuronal-glial tumor of the digestive tract: distinctive entity from gastrointestinal stromal tumor? 1194 Feb 21

This case report describes the sporadic Creutzfeldt-Jakob disease (CJD) of a 53-year-old man who initially complained about vertigo and dizziness. Within 18 weeks, he developed impaired memory, hemineglect, and sensory impairment of the left half of the body. A CSF tap was positive for 14-3-3 protein and showed increased tau protein, neuron-specific enolase (NSE), and the astroglial protein S-100 B. The EEG showed right temporal sharp waves without periodicity. Diffusion-weighted MRI revealed hyperintensities in the right temporo-occipital cortex which corresponded well with hypometabolic areas in a PET scan and the neurological and neuropsychological deficits. The morphological FLAIR T2 MRI showed no pathological changes. Within 20 weeks, the patient developed severe dementia with decreased spatial orientation and myoclonia, became incontinent, and was confined to bed. He died within 22 weeks after the first presentation of symptoms.
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PMID:[Correlation of diffusion-weighted magnetic resonance imaging with neurological deficits in sporadic Creutzfeldt-Jakob Disease]. 1221 82

A retrospective study of cerebrospinal fluid (CSF) markers of brain parenchymal damage was conducted in Vietnamese adults with severe malaria. Three markers were analysed by immunoassays: the microtubule-associated protein tau, for degenerated axons; neuron-specific enolase (NSE), for neurons; and S100B for astrocytes. The mean concentration of tau proteins in the CSF was significantly raised in patients with severe malaria compared with controls (P=0.0003) as reported for other central nervous system diseases. By contrast, the mean concentration of NSE and S100B remained within the normal range. Tau levels were associated with duration of coma (P=0.004) and S100B was associated with convulsions (P=0.006). Concentrations of axonal and astrocyte degeneration markers also were associated with vital organ dysfunction. No association was found between the level of markers of brain parenchymal damage on admission and a fatal outcome. On admission to hospital, patients with severe malaria had biochemical evidence of brain parenchymal damage predominantly affecting axons.
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PMID:Cerebrospinal fluid levels of markers of brain parenchymal damage in Vietnamese adults with severe malaria. 1593 12

Subacute spongiform encephalopathies are rare fatal diseases that affect the central nervous system, which is thought to be caused by prions, characterized clinically by a rapid progressive dementing course, along with generalized myoclonus. The prototype of these conditions in humans is Creutzfeldt-Jakob Disease (CJD). Although the final diagnosis depends on neuropathological examination, the presence of periodic sharp wave complexes on EEG and of the neuron-specific enolase, tau protein, S-100, and of the 14-3-3 protein in the cerebrospinal fluid, make the diagnosis of probable CJD. However, as these criteria are not completely accurate and the early diagnosis is extremely difficult, much interest has been focused recently on imaging methods. With the advent of diffusion-weighted imaging, MRI has shown high sensitivity and specificity, therefore being considered a useful method for the early diagnosis of this entity.
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PMID:Subacute spongiform encephalopathies. 1634 Mar 37


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