Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.1.8 (cholinesterase)
12,691 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

Changes in CSF enzyme activity were studied after brain trauma for their prognostic value. Raised values of CPK and HBDH were demonstrated in the CSF of patients with severe brain injuries. Standardised cold lesions of the brain were induced in cats. The activities of the enzymes CPK, HBDH, LDH, GOT, GPT, and pseudocholinesterase were studied at half hour intervals in the cerebrospinal fluid and at hourly intervals in the serum. A statistically highly significant increase of all enzymes studied developed in the CSF. The greatest changes occurred within four hours of freezing. Large increases could occur in half an hour. Isoenzyme studies demonstrated that CPK and LDH were of cerebral origin. No consistently significant changes could be shown in the serum enzyme activity. It is concluded that after brain injuries, enzymes are released into the extracellular fluid of the brain and transported to the CSF. The limited value of a single enzyme estimation is emphasised. The results described seem to provide indirect evidence for transependymal flow of extracellular fluid in brain oedema.
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PMID:Cerebrospinal fluid enzymes in acute brain injury. 1. Dynamics of changes in CSF enzyme activity after acute experimental brain injury. 91 9

Changes in the cholinergic, serotonergic, noradrenergic, dopaminergic, GABAergic and somatostatinergic neurons were investigated to determine their roles in Alzheimer's disease (AD). Markers for these systems were analyzed in postmortem brain samples from 20 patients with AD and 14 controls. In the CSF study, markers for the cholinergic neurons (choline esterase, ChE) and for the somatostatinergic neurons (somatostatin-like immunoreactivity, SLI) were assayed for 93 and 75 probable AD patients and 29 and 19 controls, respectively. Activity of choline acetyltransferase (CAT) was decreased by 50-85% in four cortical areas and hippocampus in patients with AD, but not in other areas of the brain, indicating a profound deficit in the function of cholinergic projections ascending from the nucleus basalis to the cerebral cortex and hippocampus in AD. Muscarinic receptor binding was reduced by 18% in the frontal cortex but not in other areas of the brain in AD. Serotonin (5HT) concentrations were reduced (by 21-37%) in hippocampal cortex, hippocampus and striatum; and 5HT metabolite levels were lowered (by 39-54%) in three cortical areas, thalamus and putamen in AD patients. Concentrations of noradrenaline (NA) were reduced (18-36%) in frontal and temporal cortex and putamen. These data imply that serotonergic and noradrenergic projections are also affected in AD but less than the cholinergic neurons. Dopamine (DA) concentrations in AD patients were reduced by 18-27% in temporal and hippocampal cortex and hippocampus, while HVA, the metabolite of DA, was unaltered. Glutamic acid decarboxylase activity was not altered in AD. SLI was decreased (28-42%) in frontal, temporal and parietal cortex, but not in thalamus and putamen in patients with AD. Frontal tangle scores correlated most strongly with cortical CAT activity reduction and less so with decreases of 5HT, NA and DA, indicating a closer correlation with the cholinergic changes and severity of AD than with other neurotransmitter deficiencies. ChE activity and SLI were reduced by 20% and 35%, respectively, in CSF of the whole group of AD patients as compared to the controls. Comparison of CSF findings between four subgroups of dementia severity indicated that the SLI was already reduced in the group of mildest AD (-31%), while ChE activity was not. Although ChE activity in CSF declined in relation to dementia severity, however, the maximal reduction was only modest (-30%). On the other hand, SLI in CSF showed only a slight further reduction (up to -41%) as the dementia become more severe.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neurotransmitter changes in Alzheimer's disease: implications to diagnostics and therapy. 198 17

Serum albumin, cholinesterase, and cholesterol were measured in ten patients with aplastic anemia and eight with myelodysplastic syndrome who received the administration of recombinant human GM-CSF. Serum albumin, cholinesterase, and cholesterol were significantly lowered by the administration of GM-CSF and recovered after the cessation of GM-CSF. These data suggest that GM-CSF impairs the biosynthesis of liver cells and that cholesterol-lowering activity of GM-CSF, which is previously reported, is due to the impairment of liver biosynthesis by GM-CSF.
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PMID:GM-CSF-mediated impairment of liver to synthesize albumin, cholinesterase, and cholesterol. 199 59

CSF neurotransmitter markers may reflect neurochemical alterations in Alzheimer's disease (AD). The best studied neurochemical deficit in AD is that of acetylcholine. Both acetylcholinesterase and butyrylcholinesterase activity have been reported to be reduced in some but not all studies of AD CSF. Studies of monoamine metabolites have also been controversial but most authors have found reduced concentrations of CSF HVA, lesser reductions in HIAA and no change in MHPG. CSF GABA concentrations have been found to be reduced in AD. Studies of CSF neuropeptides in AD have shown reduced concentrations of somatostatin and vasopressin, normal concentrations of vasoactive intestinal polypeptide and either normal or decreased concentrations of beta-endorphin and corticotropin releasing factor. Although no individual CSF neurochemical markers are specific for AD it may be possible to develop a profile of several neurochemical markers which will have enhanced specificity.
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PMID:CSF neurotransmitter markers in Alzheimer's disease. 287 17

The activity of acetyl- and butyrylcholinesterase was determined in serum and CSF of controls and patients suffering from different types of dementia. A statistically significant decrease in the activities of both esterases was observed in CSF of demented patients, however, primary degenerative and vascular dementia did not differ in their CSF cholinesterase levels. Compared to age-matched controls the serum butyrylcholinesterase activity was also significantly lowered in the overall dementia group. No typical serum and CSF cholinesterase isoenzyme pattern was found for dementia or any of its subgroups. It is concluded that the cholinesterase levels reflect metabolic alterations associated with dementia as a collective group but cannot be used for differential diagnosis of subgroups.
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PMID:Serum and CSF cholinesterase activity in various kinds of dementia. 365 53

Acetylcholinesterase, pseudocholinesterase and their molecular forms were measured in the CSF of patients affected by Alzheimer's disease and of matched neurological controls. Three different molecular forms of ChE were found in the CSF of both groups of patients, but only two of them belonged to 'true' AChE. No differences were found between Alzheimer's disease patients and neurological controls in all the examined parameters.
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PMID:Molecular forms of cholinesterases in CSF of Alzheimer's disease/senile dementia of Alzheimer type patients and matched neurological controls. 394 78

There is a growing body of evidence that the central nervous system (CNS), even in the adult animal, is capable of adaptation and reorganization not only as a result of partial damage to the CNS but also in response to stimulation. Environmental stimulation produces changes including expansion of visual cortex, increases in dendritic branching, glia and cholinesterase. Environmental stimulation also produces behavioural changes. Experimental electrical stimulation produces changes in synapse size, synaptic vesicle change, dendritic branching and changes in synaptic transmission. In man, repetitive electrical stimulation via epidural electrodes increases plasma levels of norepinephrine, epinephrine, and dopamine, and CSF levels of norepinephrine. Repetitive electrical stimulation in man dates back to 1967 and has been used for the control of pain, to improve spasticity, bladder control, motor deficit and the autonomic hyperreflexia of spinal cord injury. In addition, improvement has been reported in epilepsy, cerebral palsy, torticollis and peripheral vascular diseases. The best controlled studies are in multiple sclerosis and peripheral vascular disease, and these results will be presented in more detail.
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PMID:Rehabilitation following brain damage: some neurophysiological mechanisms. The effects of repetitive stimulation in recovery from damage to the central nervous system. 718 88

To date the evaluation of chemically-induced neurotoxic effects on humans has been dependent mostly on electrophysiological measurements, neurobehavioral tests and biological exposure assessment. However, recently attempts have been made to develop biochemical parameters in peripheral body fluids which can be easily obtained from humans and which can represent markers for the same parameters in nervous tissue. The approach of this kind is logically based on the following facts: 1) Blood cells (e.g., platelets and lymphocytes) possess some characteristics of monoaminergic neurons such as the existence of storage vesicles of monoamines, membrane neurotransmitter receptors, high affinity uptake sites and neurotransmitter-related metabolizing enzymes. 2) Leakage of nerve-specific markers from nervous tissue to peripheral body fluids may occur following damages of target neuronal cells or macromolecules. 3) Quantitative and/or qualitative alterations of peripheral biochemical markers (e.g. neurotransmitter receptors) can be induced by the regulation mechanisms of neuronal, endocrinal and immunologic interactions when the nervous functions are perturbed by various exogenous or endogenous factors. Erythrocyte acetyl cholinesterase (AChE), free erythrocyte protoporphyrin (FEP), lymphocyte neurotoxicity target enzyme (NTE), blood aminolevulinic acid dehydratase (ALA-D), and carboxyhemoglobin (CO-Hb) are well-known peripheral markers of the effects induced by organophosphates (AChE, NTE), lead (FEP, ALA-D) and carbon monoxide (CO-Hb). Many studies have been made on the effects of organic solvents, heavy metals and pesticides on neurotransmission parameters in blood cells such as neurotransmitter uptake, receptor binding and enzyme activity. This paper summarizes the present knowledge on the development and clinical applications of some peripheral biochemical markers such as neurotransmission parameters in blood cells and neuronal or glial cell marker proteins in CSF, blood and urine. The role of these peripheral biochemical markers in the assessment of environmental chemically-induced human neurotoxicity is also discussed.
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PMID:[The role of biochemical markers in peripheral body fluids in assessment of human neurotoxicity]. 791 53


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