Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The parenchymal damage of the liver after estrogen therapy for prostatic cancer, mainly treated with diethylstilbestrol diphosphate (DES-DP), was studied in the six autopsied cases, herein. The parenchymal disorder of the liver was "nonalcoholic steatohepatitis", reported by Ludwig et al., and its degree of disorder was dependent upon the administered dose of estrogen. The acceptable total dose of DES-DP was supposed to be about 150 g at maximum, according to the various degrees of damage examined histopathologically in the six cases who were administered at total doses of DES-DP from 12.6 g to 619 g. Comparison of the histopathologic damage to the liver function tests performed within 10 days before death revealed that only the serum levels of cholinesterase (ChE) were abnormally decreased, suggesting its importance to predict the degree of "nonalcoholic steatohepatitis" by monitoring of ChE.
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PMID:[Liver disorder owing to estrogen therapy in prostatic cancer, examined histopathologically in six autopsy cases]. 262 17

We have examined the value of cholinesterase (ChE) that indicates the preservation ability of liver function, to assess the liver disorder owing to diethylstilbestrol diphosphate (DES-DP) administration in 25 prostatic cancer patients without castration. The correlation between ChE and the other factors such as age, total dose of DES-DP, duration of administration or ratio (total dose/duration), were studied by means of multiple regression analysis (MRA). In sixteen patients treated for less than 6 months, ChE was correlated with all factors by MRA with the coefficient of 0.645, and the coefficients of simple correlation between ChE and total dose and between ChE and administered duration, were -0.521 (p less than 0.05) and -0.596 (p less than 0.05), respectively. In nine patients treated for more than 6 months, ChE was correlated with all factors by MRA with the coefficient of 0.803, and the coefficient of simple correlation between ChE and ratio was -0.707 (p less than 0.05). According to these results and the permissible range of ChE, the total dose of administration for less than 6 months was estimated to be under 50 gram and its duration was within 100 days. The ratio in patients administered for more than 6 months was under 300 mg/day. Therefore, as far as the long-term hormonal treatment for prostatic cancer and preservation of liver function, we concluded that total dose of DES-DP should be less than 50 gram in less than 100 days for induction therapy and the daily dose of DES-DP should be less than 300 mg/day for maintenance therapy.
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PMID:[Liver disorder owing to estrogen therapy in prostatic cancer. The correlation between serum level of cholinesterase and dose of diethylstilbestrol diphosphate]. 262 18

Alzheimer disease (AD) involves neuronal degeneration with impaired cholinergic transmission in the cerebral cortex and hippocampus in areas of the brain particularly associated with memory and higher intellectual functioning. Other neurotransmitter deficits also occur, but the mechanisms underlying the widespread impairment of synaptic functions remain uncertain. Research on the molecular basis of AD has elucidated a pathogenic pathway from which a range of rational pharmacological interventions has emerged. Although at least 3 cholinesterase inhibitors (tacrine hydrochloride, donepezil, and rivastigmine tartrate) are now available and provide patients with modest relief, the most promising strategy involves approaches to retarding, halting, or preventing the formation or accumulation of beta-amyloid (Abeta) plaques. Estrogen is believed to have antioxidant or other anti-Abeta effects, as hormonal replacement therapy in women with menopause is associated with a reduced risk or delayed onset of AD. The association between nonsteroidal anti-inflammatory drugs and a reduced risk of AD has not yet been confirmed, but these agents may protect the brain from the reactive glial and microglial responses associated with Abeta deposition. Also, recent studies suggested that antioxidants, such as vitamin E taken alone or in combination with selegiline hydrochloride, can delay the progression of AD. Despite these encouraging results, no current therapy has been shown to halt or reverse the underlying disease process. The proof of the principle that anti-Abeta drugs will work in the transgenic models of AD is eagerly awaited with the expectation that they will eventually prove successful in humans.
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PMID:Prospects for pharmacological intervention in Alzheimer disease. 1076 17

Mutations in ric-3 (resistant to inhibitors of cholinesterase) suppress the neuronal degenerations caused by a gain of function mutation in the Caenorhabditis elegans DEG-3 acetylcholine receptor. RIC-3 is a novel protein with two transmembrane domains and extensive coiled-coil domains. It is expressed in both muscles and neurons, and the protein is concentrated within the cell bodies. We demonstrate that RIC-3 is required for the function of at least four nicotinic acetylcholine receptors. However, GABA and glutamate receptors expressed in the same cells are unaffected. In ric-3 mutants, the DEG-3 receptor accumulates in the cell body instead of in the cell processes. Moreover, co-expression of ric-3 in Xenopus laevis oocytes enhances the activity of the C.elegans DEG-3/DES-2 and of the rat alpha-7 acetylcholine receptors. Together, these data suggest that RIC-3 is specifically required for the maturation of acetylcholine receptors.
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PMID:The C. elegans ric-3 gene is required for maturation of nicotinic acetylcholine receptors. 1186 29

Development of dementia depends on genetic susceptibility and on risk factors accessible to primary prevention. Among the latter, vascular risk factors are well defined: prevention of hyperhomocysteinemia, diabetes mellitus, hypercholesterolemia, and, to some extent, of arterial hypertension could avoid the cognitive decline of dementia. Estrogen replacement therapy, antiinflammatory drugs, alcohol, vitamin E and intellectual activities seem efficacious in term of primary prevention. When dementia is present, only vitamin E, selegiline and some antiinflammatory drugs have proved efficacy compared to placebo to slow the cognitive decline. Long-term effects of cholinesterase inhibitors need to be investigated in future trials.
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PMID:[Prevention of dementia: is it possible?]. 1286 24

Alzheimer's disease is the most common dementia disorder characterized by multiple pathological changes in the brain leading to a progressive memory loss and other cognitive symptoms producing occupational and social disabilities. Although a great deal of progress has been made in recent years in further understanding the genetic aberrations and patho-physiological processes of Alzheimer's disease there is still no cure of the disease. The transmitter replacement therapy is so far the most explored therapy. Three cholinesterase inhibitors have so far been approved and presently in clinical use in many countries. Although the cholinesterase inhibitors generally appear to produce symptomatic effects with palliative effect on existing cognitive disturbances recent data suggest that they also may have effect on progression of the disease including possible neuroprotective effects. Possible interactions between Abeta and cholinergic neurotransmission may exist. Treatment of cells with Abeta causes decreased cholinergic activity. Pretreatment of PC12 cells with cholinesterase inhibitors such as tacrine and donepezil in clinical relevant concentrations can attenuate Abeta (25-35) toxicity through mechanisms which may be mediated via nicotinic receptors. Estrogen has been shown to protect against Abeta toxicity in different cell lines and also to reduce the formation of Abeta. Its mechanism for the neuroprotective effect is however not fully clarified. A potentiation of the clinical effect of cholinesterase inhibitors in Alzheimer patients has been given together with estrogen. Experimental data suggest that the neuroprotective effect of estrogen as studied in PC12 cells was mediated at least partly via the alpha(7) nicotinic receptor. Treatment with Abeta in nanomolar concentrations for 7 days in PC12 cells significantly decreased the number of nicotinic receptor binding sites and mRNA levels. The effects by Abeta on nicotinic receptors are prevented by nicotine pretreatment. The finding suggests a possible link between Abeta and nicotinic receptor deficits in Alzheimer patients in the early course of the disease.
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PMID:Neuroprotection in Alzheimer's disease - new strategies for treatment. 1678 38

As the transgender patient population continues to grow, health care providers will need to become aware of elements unique to the transgender community in order to provide the highest quality of care. Neuromuscular blockade with succinylcholine is routinely administered to patients undergoing electroconvulsive therapy (ECT). Decreased amounts or activity of pseudocholinesterase in serum can lead to prolonged duration of muscle paralysis. Causes of reduced action by pseudocholinesterase include genetically abnormal enzymes, reduced hepatic production, pregnancy, and various drug interactions. Estrogen supplementation taken by transitioning patients may affect the duration of neuromuscular blockade.This is a case of a 32-year-old male-to-female transgender patient with prolonged apnea following ECT treatment for severe, refractory depression. Further investigation revealed the patient was on estrogen therapy as a part of her transition and laboratory testing demonstrated reduced serum pseudocholinesterase activity. Further laboratory testing demonstrated reduced serum pseudocholinesterase activity. Succinylcholine dosing was titrated to an appropriate level to avoid prolonged apnea in subsequent ECT treatments. Physicians and other health care providers are faced with a unique population in the transgender community and must be aware of distinctive circumstances when providing care to this group. Of specific interest, many transitioning and transitioned patients can be on chronic estrogen supplementation. Neuromuscular blockade in those patients require attention from the anesthesiology care team as estrogen compounds may decrease pseudocholinesterase levels and lead to prolonged muscle paralysis from succinylcholine.
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PMID:Electroconvulsive Therapy Considerations for Transgendered Patients. 2800 18