Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The report pertains to some data on the cholinesterase activity in the blood serum and CSF of 62 patients with epilepsy, in correlation with different clinical characteristics (the severity of the disease, the character of the EEG, frequency of seizures, treatment efficacy, etc). In 86,8% of the cases there was a significant increase in the activity of serum cholinesterase. Increased cholinesterase activity correlated only with pronounced pathological changes in the EEG (reverse correlation) and the efficacy of treatment (direct correlation). After surgical treatment of 9 cases there was a drop in the cholinesterase activity of the blood serum and CSF, which correlated with an improvement in the general state of the patients. On the basis of personal experience, as well as literary data, it is assumed that an increase in the cholinesterase activity in epileptic patients is not related to the main etiological factors of this disease but is rather a secondary change, a peculiar "symptom" of the disease.
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PMID:[Role of the acetylcholine--cholinesterase system in the development of epilepsy]. 47 14

Acetylcholinesterase (AChE) activity in dog plasma is significantly higher than in either ventricular or cisternal CSF. However, since protein levels in plasma are about 100-fold higher than in CSF, the specific activity of AChE is lower in plasma than in CSF. Acetylcholinesterase activity in plasma represents only 22% of total cholinesterase (ChE) activity, while preliminary findings indicate that in ventricular CSF it is 50-60%. Acetylcholinesterase activity in ventricular CSF is significantly lower than in cisternal CSF. Chlorpromazine (10 mg/kg, intravenous), a drug which increases acetylcholine turnover, increased AChE-specific activity in all dogs. Our results support the hypothesis of a neuronal origin of AChE activity in CSF.
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PMID:Acetylcholinesterase activity in ventricular and cisternal CSF of dogs: effect of chlorpromazine. 73 56

Previous investigators have detected unknown oxidized forms of 5-hydroxytryptamine (5-HT) in the CSF of Alzheimer's disease (AD) patients. Furthermore, an unidentified autoxidation product of this neurotransmitter is an inhibitor of acetylcholinesterase (AChE), an enzyme compromised in the Alzheimer brain. In this study it is demonstrated that the major product of autoxidation of 5-HT is 5,5'-dihydroxy-4,4'-bitryptamine (DHBT). Central administration of DHBT to mice at a dose of 40 micrograms (free base) evokes profound behavioral responses, which persist until the animals die (approximately 24 h). One hour after central administration of DHBT, the levels of norepinephrine, dopamine, 5-HT, and acetylcholine and their metabolites in whole brain are greatly elevated. Disturbances to the catecholaminergic and serotonergic systems were still evident shortly before the death of animals. DHBT is also shown to be a noncompetitive inhibitor of AChE in vitro. These observations suggest that if DHBT is formed as an aberrant metabolite of 5-HT in the human brain, it could potentially be neurotoxic and contribute to the neuronal degeneration and other neurochemical and neurobiochemical changes associated with AD or perhaps other neurodegenerative diseases.
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PMID:5,5'-Dihydroxy-4,4'-bitryptamine: a potentially aberrant, neurotoxic metabolite of serotonin. 135 95

We used the ELISA to measure the concentration of amyloid protein precursor with Kunitz type trypsin inhibitor domains (APPI) in CSF of dementia of the Alzheimer type (DAT) and examined the correlation of APPI with acetylcholinesterase (AChE) and somatostatin (SRIF). We found the APPI concentration in CSF of DAT to be significantly elevated compared with that of multi-infarct dementia and controls. We could significantly correlate APPI with AChE, but not correlate APPI with SRIF. The present results suggest that measurement of CSF APPI levels may be useful for diagnosis of DAT and the change of APPI may closely be associated with abnormality of acetylcholine system in DAT that has been reported.
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PMID:Amyloid beta protein precursors with kunitz-type inhibitor domains and acetylcholinesterase in cerebrospinal fluid from patients with dementia of the Alzheimer type. 137 55

We studied the effect of aging on EEG spectra recorded from T5-O1 (T6-O2) derivation. The aging series composed of 52 normal individuals aged 20 to 91 years. Seventy-nine per cent of visual and 81% of quantitative EEGs were considered normal. The absolute amplitude of delta and theta bands and absolute power of delta band were lower for the oldest group (aged 60 and over) than for the youngest group (aged 20-39 years). Age was inversely related to the amount of delta and theta indicating that the amount of slow activity in quantitative EEG does not increase with age in the context of good health status. Women had more beta activity compared with men. In addition, the amount of beta and alpha bands showed tendency for a reduction with age. Fifteen subjects aged 50 years or older participated in a 2-year follow-up including EEG and neuropsychological evaluation. Seven of them deteriorated in learning ability and showed increase in delta activity. In the oldest age group, delta amplitude was positively correlated with intrusion errors in the list learning test and inversely related to acetylcholinesterase activity of the CSF. Thus, a link between the cholinergic system, EEG slowing and memory problems in old age is suggested.
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PMID:Aging and spectral analysis of EEG in normal subjects: a link to memory and CSF AChE. 141 24

We have devised a simultaneous assay system for megakaryocyte colony-stimulating factor (Meg-CSF) and megakaryocyte potentiator (Meg-Pot) by modifying a quantitative measuring technique for acetylcholinesterase activity (Ach-E) of megakaryocytes by automatic colorimetry using microplates. We cultured murine bone marrow cells treated with diisopropyl fluorophosphate in a serum-free system with serum-free pokeweek mitogen-stimulated spleen cell conditioned medium (PWM-SCM) and an unknown factor, preparing two microplates with the identical culture system. In the first plate, the total number of Ach-E-positive cells induced solely by the factor tested was indicative of Meg-CSF activity and additive increases in this parameter on simultaneous addition of PWM-SCM and the factor tested were indicative of early Meg-Pot activity. Total Ach-E activity (total change at optical density of 414 nm) per well was measured in the second plate to calculate total change at optical density of 414 nm per megakaryocyte, an indicator of late Meg-Pot activity. With this system, recombinant human erythropoietin showed both Meg-CSF and early and late Meg-Pot activities in in vitro megakaryopoiesis. Recombinant murine granulocyte-macrophage colony-stimulating factor possessed weak Meg-CSF and early Meg-Pot activity, whereas recombinant human granulocyte colony-stimulating factor exhibited late Meg-Pot activity and thrombocytopenic serum exhibited early and late Meg-Pot activities. This assay system is useful in screening Meg-CSF or Meg-Pot activities in unknown factors.
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PMID:Simultaneous assay for megakaryocyte colony-stimulating factor and megakaryocyte potentiator and its application. 169 13

Chromogranin A (CgA) is co-released with catecholamines and peptides and has a wide distribution in the brain. Chromogranin A provides a measure of tonic arousal. CSF CgA-like immunoreactivity (CgA-LI) was studied in 42 drug-free male schizophrenic patients. 33 of these patients were first studied during chronic haloperidol maintenance treatment. Withdrawal from haloperidol maintenance treatment was associated with a significant increase in CSF CgA-LI, particularly in the patients who did not relapse. Contrary to expectation CSF CgA-LI was higher in drug-free patients who slept longer the night before the lumbar puncture. Significant relationships were observed between CSF CgA-LI and CSF homovanillic acid, acetylcholinesterase, neuropeptide Y-LI and 5-hydroxy-indole acetic acid, but not with CSF norepinephrine or 3-methoxy-4-hydroxyphenylglycol. Ventricular brain ratios correlated negatively with CSF CgA-LI levels.
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PMID:CSF chromogranin A-like immunoreactivity in schizophrenia. Assessment of clinical and biochemical relationships. 172 93

Cerebrospinal fluid acetylcholinesterase (CSF AChE) was determined for elderly delirious patients during the acute stage and after a 1-year followup, and the AChE levels were compared with those of age-equivalent controls. At the acute phase, the AChE levels of the delirious patients were in the same range as those of the control group, but during the followup, a slight declining trend was observed. These results do not unambiguously support the previously suggested role of cholinergic dysfunction in the pathogenesis of acute delirium, although the augmented striatal release of AChE in hyperkinetic and mixed delirium may mask the involvement of cholinergic neurons.
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PMID:A longitudinal study of cerebrospinal fluid acetylcholinesterase in delirium: changes at the acute stage and at one-year followup. 175 28

Ganglioside AGF2 prevented the cognitive and locomotor alterations induced by intraventricular colchicine. Adult male rats were initially trained to perform a standard radial arm maze (RAM) task. Following training, they were injected intraperitoneally with 10 mg/kg AGF2 (COL/AGF2), cerebrospinal fluid (CSF/AGF2) or the saline vehicle (COL/SAL, CSF/SAL) for 3 days prior to and for 14 days following the bilateral injection of colchicine (7 micrograms/0.5 microliters) or artificial CSF into the lateral ventricles. Colchicine (COL/SAL) impaired performance of the standard RAM task as well as a working memory version of the task in which various delays were imposed between the fourth and fifth arm choices. Colchicine also produced a transient hyperactivity which subsided within 10 weeks following surgery. In contrast, AGF2 (COL/AGF2) prevented the impairments in RAM performance and the alterations in locomotor behavior. Colchicine also produced significant decreases in hippocampal ChAT activity and high affinity choline uptake that were prevented by prior treatment with AGF2. Finally, colchicine produced a 35% decrease in the number of acetylcholinesterase-positive (cholinergic) neurons in the medial septum and vertical limb of the diagonal band (MS/VLDB) which was also prevented by AGF2. Thus, the behavioral and neurochemical protection afforded by AGF2 was paralleled by a prevention of the loss of hippocampal cholinergic parameters and cholinergic neurons in the MS/VLDB.
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PMID:Ganglioside AGF2 prevents the cognitive impairments and cholinergic cell loss following intraventricular colchicine. 202 33

To investigate the effect of recombinant granulocyte-macrophage colony-stimulating factor (rGM-CSF) on murine megakaryocytopoiesis in vitro, the factor was added to both serum-free colony assays and liquid marrow cultures. GM-CSF had a significant megakaryocytic colony-stimulating activity. After 2 hours of preincubation with and without 10 ng/mL rGM-CSF, the percentage of megakaryocyte colony-forming cell (CFU-MK) in DNA synthesis was determined by tritiated-thymidine suicide using colony growth. The reduction of CFU-MK colony numbers in marrow culture was 47.5% +/- 9.9%, 20.9% +/- 5.2% (control), respectively, indicating that the factor affected cell cycle at CFU-MK levels. When acetylcholinesterase (AchE) production was measured fluorometrically after 4 days of liquid culture, rGM-CSF elicited an increase in AchE activity in a dose-dependent fashion. To determine if the hematopoietin acts directly on megakaryocytic differentiation, 2 ng/mL rGM-CSF was added to serum-free cultures of 295 single megakaryocytes isolated from CFU-MK colonies. An increase in size was observed in 65% of cells initially 10 to 20 microns in diameter, 71% of cells 20 to 30 microns, and 40% of cells greater than 30 microns. Conversely, in absence of GM-CSF, 17%, 31%, and 10% of cells in each group increased in diameter. These data suggest that rGM-CSF promotes murine megakaryocytopoiesis in vitro and that the response to the factor is direct. To determine if the factor influences megakaryocytic/thrombocytic lineage in vivo, 1 and 5 micrograms of rGM-CSF were administered intraperitoneally every 12 hours for 6 consecutive days. Although a two- to three-fold increase in peripheral granulocytes was observed, neither megakaryocytic progenitor cells or platelets changed. Histologic analysis of bone marrow megakaryocytes showed no increase in size and number. The in vivo studies demonstrated no effect of GM-CSF on thrombocytopoiesis. The discrepancies between the in vitro and in vivo effects of GM-CSF require additional investigations.
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PMID:Effect of recombinant granulocyte-macrophage colony-stimulating factor on murine thrombocytopoiesis in vitro and in vivo. 218 Apr 95


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