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

As many as 94 women of reproductive and climacteric age were subjected to clinical and laboratory studies. Women of reproductive age demonstrated abnormalities of menstrual function of the type of ovulatory and anovulatory hemorrhages. The group over 40 years manifested an early onset of menopause. Alcoholism standing was from 2 to 15 years. Study of the neurohumoral characteristics in women suffering from alcoholism during abstinence revealed a considerable lowering of serotonin content in the blood as compared with normals. The content of acetylcholine, the activity of genuine and false blood cholinesterase were increased in women suffering from alcoholism, pointing to excitation in the cholinergic system. During abstinence, women of reproductive and climacteric age suffering from alcoholism demonstrated discrepancy in the activity of the neuromediator systems.
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PMID:[Clinical and neurohumoral indicators in women-alcoholics of reproductive and climacteric age]. 216 Jan 75

The cholesterol and phospholipid content and the fatty acid composition in plasma and red cell membranes was determined in 10 alcoholics with macrocytic erythrocytes. None of the patients had anemia. Red cells exhibited macrocytosis up to 108 fl in all patients. Bilirubin, albumin, prothrombin, and cholinesterase were in the normal range, whereas transaminases and gamma-glutamyl transpeptidase activities in serum were elevated in most of the patients. The molar ratio cholesterol/phospholipids in red cells was not altered in alcoholics. An abnormally high ratio of saturated/unsaturated fatty acids was found in plasma as well as in red cell phospholipids from alcoholics. Linoleic acid was substantially decreased in plasma of alcoholics (controls 32.3%, alcoholics 21.8%). This fatty acid abnormality was reflected by a decrease of linoleic acid in red cell phosphatidylcholine. The present data may suggest that fatty acid changes taking place in membranes of macrocytes were a consequence of changes in the plasma and reflect plasma/membrane exchanges rather than direct effects of ethanol on red cell membranes. Lipid alterations of red cell membranes may be involved in the development of macrocytosis in chronic alcoholism.
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PMID:Plasma and red cell lipids in alcoholics with macrocytosis. 371 88

Cholinergic neurotransmission has been followed in striatum and hippocampus in two inbred strains of mice (C57Bl/6 and Balb/c) during long term alcohol exposure (over a 25 month period) and with aging. Marked strain dependent differences in reactivity of pre- and postsynaptic cholinergic markers to chronic alcohol exposure and aging were demonstrated in both structures. The Balb/c strain exhibits a remarkable long lasting tolerance to alcohol injury for striatal and hippocampal cholinergic markers (choline acetyltransferase, high affinity choline uptake, muscarinic receptors affinity, acetyl cholinesterase), whereas C57Bl mice appear more sensitive to alcohol intoxication. Likewise aging affects the C57Bl mouse more severely than the Balb/c, a phenomenon which may be involved in the sensitivity of these mice to alcohol intoxication. Moreover long term alcohol exposure, in addition to aging show unequal effects on the diverse cholinergic markers studied. Also divergences of specific brain areas have been noted and should be related to their particular neuroanatomy. Such discrepancies may, in part, explain differences observed in the behavioral effects of chronic alcohol intoxication in alcoholics.
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PMID:Influence of mouse genotype on responses of central cholinergic neurotransmission to long term alcohol intoxication. 377 44

An increase in content of acetylcholine (AC) as well as stimulation of choline acetyltransferase and acetylcholinesterase were observed in basal ganglia of rat brain during development of alcohol dependency, thus indicating the activation of the AC structures. Less distinct activation of the AC structures occurred in limbic (frontal) cortex. At the step of complete alcohol dependency the patterns of AC metabolism were considerably normalized in the both brain structures; at the same time, activity of the gamma-aminobutyric acid (GABA) system was decreased, which occurred due to inhibition of the GABA synthesis. At the III step of experimental alcoholism with "physical" dependency on ethanol synthesis and release of the AC were lowered, especially distinct in basal ganglia. These phase alterations in the activity of the AC structures in basal ganglia were accompanied by the similar alterations in content of glutamate: an increase of glutamate at the I step of alcoholism and a decrease--at the III step. Possible mechanisms and pathogenetic role of the phase alterations observed in metabolism of the brain neurotransmitters and in activity of AC- and GABA-structures during development of alcohol dependency are discussed. The data obtained suggest that the specific steps of alcoholism should be taken into consideration in the differential treatment using neurotransmitter drugs.
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PMID:[Metabolism of acetylcholine and gamma-aminobutyric acid in the basal ganglia and limbic cortex of rats at different stages in the development of alcohol dependence]. 395 3

Eighteen patients with chronic alcoholism, stages II-III were examined during tisercin treatment and medicamental interval. In patients with stage II alcoholism, perversion of the central neuronal tisercin effect was shown. Phenothiazines efficacy during abstinence period appeared to be linked with the perversion observed. Individual constant control of blood pressure, heart rate, acetylcholinesterase serum level, sleep function etc. during drug treatment is considered to be a perspective trend for an increase of toxicomania treatment efficacy.
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PMID:[Principles for evaluating reactivity in the clinical picture of alcoholism and addiction during drug therapy]. 685 84

Plasma aromatic amino acid (AAA) and branched-chain amino acid (BCAA) concentrations were determined in 292 alcoholics. The BCAA/AAA molar ratio in patients with alcohol withdrawal symptoms was compared with the ratio in patients without such symptoms. The BCAA/AAA molar ratio in patients with transient hallucinations or with delirium tremens was significantly lower than that in patients without these symptoms. The BCAA/AAA molar ratio tended to be lower in patients with alcohol withdrawal seizures than in patients without such symptoms. The BCAA/AAA molar ratio had a negative correlation with plasma total bilirubin and LDH, and a positive correlation with plasma cholinesterase and albumin. These results indicate that abnormalities of amino acid metabolism caused by liver damage in alcohol dependence may have an important role in the pathogenesis of the alcohol withdrawal syndrome.
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PMID:Aromatic and branched-chain amino acid levels in alcoholics. 906 12

The management of dementia patients encompasses pharmacologic, behavioral, and psychosocial intervention strategies. Before pharmacologic intervention is instituted, it is important that sources of excess disability and comorbidity be eliminated or reduced. Identification of comorbid medical and psychiatric conditions, such as depression and delirium, should be identified and appropriately treated. Providing caregivers with education, support, and practical advice is a critical component of the management of the demented patient. The current standard of care for pharmacologic management of the cognitive and functional disabilities of AD consists of the combination of a cholinesterase inhibitor and high-dose vitamin E. This standard is based on the results of large-scale, double-blind, placebo-controlled trials. Cholinesterase inhibitors are the only FDA-approved pharmacologic treatments for AD. Cholinesterase inhibitors have been shown to be effective in the treatment of the cognitive, behavioral, and functional deficits of AD. Large-scale placebo-controlled trials of tacrine, donepezil, rivastigmine, and galantamine have demonstrated moderate benefits in patients with mild to moderate AD. Donepezil, rivastigmine, and galantamine are the first-line choices in the treatment of AD because of their lack of hepatotoxicity, ease of administration, few significant drug-drug interactions, and mild to moderate side effects. There are few contraindications to the use of cholinesterase inhibitors. Known hypersensitivity to a specific drug or its derivatives is the only true contraindication. Cautious administration of cholinesterase inhibitors is advised in patients who have a previous history of allergy or adverse reactions to prior cholinesterase inhibitors, severe liver disease, preexisting bradycardia, peptic ulcer disease, current alcoholism, asthma, or chronic obstructive pulmonary disease. Nausea, vomiting, diarrhea, and anorexia are the most common side effects of cholinesterase inhibitors. These gastrointestinal side effects can be minimized by gradual dose increases, administration with food, adequate hydration, and judicious use of an antiemetic. Vitamin E has been demonstrated to slow the progression of AD in several small and one large placebo-controlled trials. Because of its low cost and safety, it is recommended in addition to a cholinesterase inhibitor for the treatment of AD. There are no FDA-approved treatments for DLB and VaD. One small placebo-controlled trial demonstrated that rivastigmine may be effective in the treatment of DLB. More large-scale placebo-controlled trials are needed to confirm the results of this study. Treatment of VaD focuses on the control, identification, and management of cerebrovascular disease and vascular risk factors. Although there are no peer-reviewed reports on the efficacy of cholinesterase inhibitors for VaD or mixed AD/VaD, early reports suggest that these agents may also be effective for mixed AD/VaD. The indications for the use of cholinesterase inhibitor drugs are eventually likely to broaden to include DLB, mixed AD/VaD, and AD in its more advanced stages.
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PMID:Pharmacologic treatments of dementia. 1217 Oct 61

The main thrust of the meeting was, as always, basic research in behavioral neuroscience defined in a broad sense. Learning and memory, feeding and drinking, reward mechanisms, development of the CNS, anxiety and stress were the main topics covered. In a public lecture associated with the meeting, Larry Reid (Rensselaer Polytechnic Institute, Troy, NY, USA) reviewed the quite compelling evidence in favor of the effectiveness of naltrexone for preventing relapse in former alcoholics. He also presented preclinical data demonstrating the remarkable effects of naltrexone given together with isradipine (Novartis AG) in blocking the rewarding effects of cocaethylene. This combination of drugs could thereby constitute a treatment for alcoholism complicated by cocaine abuse. Of potential therapeutic interest was also the description of the preclinical pharmacology and a phase II trial of a new cholinesterase inhibitor, methanesulfonyl fluoride (University of Texas). The possible physiological functions of sigma opioid receptors and the pharmacological properties of sigma receptor ligands were discussed at one of the symposia. Among the subjects covered were the potential use of sigma1 antagonists in the treatment of cocaine addiction and the efficiency of sigma1 agonists for preventing the decline in cognitive functions associated with old age.
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PMID:International Behavioral Neuroscience Society - ninth annual meeting. 1608 41

A cluster of Guillaine-Barre syndrome cases in the Vaalharts region, South Africa prompted an investigation of the impact of aerial organophosphate spraying on cholinesterase levels of residents in the region. A prospective study of cholinesterase levels among residents and workers in the area and a control area was performed. Standardized red blood cell cholinesterase levels amongst participants were monitored before (round 1), during (round 2), and after (round 3) the 1996/1997 aerial spraying season. Participants were assigned environmental exposure categories based on the time since (within 10 or 30 days) and distance from (on farm, on neighboring farm, <10 km from farm) aerial pesticide application. There were 342 participants in round 1, of whom 78% participated in round 2, 62% in round 3, and 56% in all three rounds. There was an increase in cholinesterase levels in round 2 (mean increase = 5.96+/-6.25 IU/g hemoglobin) and then a decrease in round 3 (6.17+/-6.51), significantly associated with environmental exposure (participants living on farm or neighboring farm and <10 km from spraying area) controlling for age, gender, alcohol dependence, and usual and recent domestic and occupational pesticide use (e.g., for round 2-round 1 cholinesterase differences, beta; (exposed group relative to unexposed)=5.72+/-1.21 IU/g hemoglobin, P = 0.000, R2 = 0.27, n = 171). The results show a shift in cholinesterase levels associated with residence in the spraying area, but in the direction opposite to that expected from the spraying of pesticides. Seasonal fluctuations in ambient temperature during the study may have influenced the results.
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PMID:The impact of aerial application of organophosphates on the cholinesterase levels of rural residents in the Vaalharts district, Northern Cape Province, South Africa. 1656 70

Alcohol abuse is a health problem throughout the world and alcohol consumption is linked to the occurrence of several pathological conditions. Acute ethanol administration exerts a variety of actions on the central nervous system (CNS). Zebrafish has been used as an attractive model system to investigate behavioral and neurochemical changes promoted by alcohol intoxication. Here we investigated the in vitro and in vivo effects promoted by ethanol and its metabolites on zebrafish brain acetylcholinesterase (AChE). There was a significant increase of AChE (33%) activity after acute 1% ethanol exposure. However, ethanol in vitro did not alter AChE activity. Acetaldehyde, the first metabolite of alcohol metabolism, promoted a dose-dependent decrease (15%, 27.5% and 46.5%) at 0.25%, 0.5% and 1%, respectively. Acetate, a product of acetaldehyde degradation, did not change AChE activity. Furthermore, the acute ethanol exposure was able to inhibit AChE transcripts at 0.5% and 1%. These findings suggest that the alterations on zebrafish AChE could reveal molecular mechanisms related to cholinergic signaling in alcoholism.
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PMID:Ethanol alters acetylcholinesterase activity and gene expression in zebrafish brain. 1788 94


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