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:3.1.1.7 (acetylcholinesterase)
28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The levels of norepinephrine, dopamine and 5-hydroxytryptamine in brain homogenates of vitamin B12-deficient rats have been investigated. The norepinephrine levels were significantly decreased in the deficient animals compared to controls. The two major catabolic pathways of norepinephrine e.g. monoamine oxidase and catechol-O-methyl transferase did not show significant variations. Both acetyl cholinesterase and butiryl-cholinesterase markedly decreased in the plasma of the vitamin B12-deficient rats.
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PMID:Levels of neurotransmitters in brain of vitamin B12 deficient rats. 1 22

State-of-the-art precision values are presented for the following serum constituents: aldolase (EC 4.1.2.13), alpha-hydroxybutyrate dehydrogenase (EC 1.1.1.30), cholinesterase (EC 3.1.1.8), cortisol, gamma glutamyl transferase (EC 2.3.2.2), haptoglobin, immunoglobulins, lactic acid, leucine aminopeptidase (EC 3.4.1.1), total lipids, osmolality, protein fractions, T3 uptake, thyroxine and vitamin B12. Precision estimates are based on values reported for four lyophilized serum pools analyzed by participants in the Pennsylvania Association of Clinical Pathologists regional quality control program for clinical chemistry, during 1976, 1977 and 1978. Use of the upper limit of the "most common range" of precision (that range including the 75 percent most precise laboratories) as a warning level for trouble-shooting is advocated.
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PMID:Additional day-to-day precision estimates based on regional chemistry quality control data. 51 9

In an analysis of the gastrocnemius muscle, the microsomal fraction showed the highest cholinesterase (ChE) activity. The ChE activity of all fractions decreased to a greater extent after strong nerve crushing than after weak crushing. This change in the activity in the microsomal fraction was the most marked change observed. Although in the analysis of the soleus muscle the ChE activity was measured only in the homogenate and in the microsomal fraction, the results were the same as those obtained with the gastrocnemius. A preparation of vitamins B1, B2, and B12 (B complex) had little effect on the ChE activity in the gastrocnemius muscle. In the soleus muscle on the lesion side, the B complex increased the ChE activity to some extent after nerve crushing, but such was not significant. However, the B complex signifiicantly increased this activity in the soleus on the intact side. In the soleus muscle, strong nerve crushing induced more marked muscle atrophy than weak crushing. On the other hand, no significant difference was found in the gastrocnemius. Effects of the B complex on muscle atrophy were found in the soleus, but not in the gastrocnemius. These results suggest that the ChE activity in the microsomal fraction containing sarcoplasmic reticulum reflects the nervous disorders clearly, and that the B complex increases the ChE activity and muscle weight in the soleus, but not in the gastrocnemius muscle.
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PMID:[Changes in cholinesterase activity of gastrocnemius and soleus muscles of the rat after crush of the sciatic nerve, and effects of a vitamin B complex on those changes (author's transl)]. 75 Mar 31

We studied the nutritional status and the prevalence of malabsorption in 12 patients one to three years after total gastrectomy (TG) for gastric neoplasm. The Roux-en Y technique was used for reconstruction. A correct dietary regimen according to the recommended daily allowance was suggested and patients were seen quarterly on an out patient basis. The nutritional status was evaluated by measuring serum albumin levels, total iron binding capacity, cholinesterase, area muscular circumference, triceps skinfold and delayed hypersensitivity response. Work-up studies for the small intestine included: stool fat, D-xylose and glucose tolerance tests, Schilling test (phase II and III), serum iron levels, serum vitamin B12 levels and biopsy of the jejunum. Malnutrition, defined as the occurrence of two or more abnormal nutritional parameters, was observed in one patient; glucose and D-xylose tolerance tests were normal in all. A mild degree of steatorrhea was observed in four patients. The second phase of the Schilling test was abnormal in eight patients, but urinary excretion of vitamin B12 increased in three of four patients after use of antibiotics. Low serum vitamin B12 levels were common after the twentieth postoperative month. Serum iron levels were initially low and returned to normal six months after TG. All patients had normal jejunal histologic findings. These data indicate that malnutrition after TG is not common if an adequate dietary intake is maintained. Malabsorption, possibly due to bacterial overgrowth, is not a major clinical problem.
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PMID:Nutritional status, function of the small intestine and jejunal morphology after total gastrectomy for carcinoma of the stomach. 375 Jan 77

In 1992 people aged 65 years and over represented 11.9% (men) and 17.2% (women) of the Swiss population, and in 2000 the average 65-year-old man or woman can expect to live about 12 more years. Old age is characterized by multimorbidity, an accumulation of chronic conditions and diseases, and by social isolation. Multimorbidity and isolation (living alone) are the major risk factors for malnutrition. 30-60% of all persons aged 65 years and over show one or more subnormal nutritional parameters. The unspecific and oligosymptomatic clinical picture of malnutrition in the elderly often hinders an early diagnosis, and malnutrition is often misdiagnosed as "wasting away syndrome" of the old. Thus, the nutritional assessment of the elderly should become a routine diagnostic procedure. Detection of malnutrition involves assessment of nutritional parameters including history (eating habits, appetite), anthropometric measurements (weight, height, body mass index, triceps skinfold, midarm circumference), serum proteins (albumin, transferrin, prealbumin, cholinesterase, retinol binding protein), vitamins (B12, folic acid, B1, B2, B6, C and D), minerals and trace elements (zinc, magnesium, calcium, iron), immunologic skin tests and lymphocyte count. Depending on the history and the clinical symptoms, a selected number of these nutritional parameters are assessed. When assessing the nutritional status of the elderly it is important to define the etiologic factors involved. Thus, treatment of underlying causes and refeeding can be streamlined, so that maximum benefit can be obtained for the quality of life of the elderly.
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PMID:[Special aspects of malnutrition in geriatrics]. 787 97

Alzheimer's disease (AD) is associated with a reduction in cholinergic activity as a result of specific neuronal loss. Current potential treatments for the disease include both cholinomimetic drugs and anticholinesterase inhibitors. One of the drugs approved by the FDA is tacrine (9-amine-1,2,3,4 tetrahydroacridine; THA), a strong acetylcholinesterase (AChE) inhibitor. We have studied the effects of tacrine on glial and neuronal cells in culture assessing cell survival and viability and morphology. Lactate dehydrogenase (LDH) activity and methylthiazol-diphenyl-tetrazolium (MTT) reduction were used as toxicity indicators. We found that tacrine toxicity on rat B12 glial cells and mouse Neuro 2A cells was strongly dependent on its concentration (up to 500 microM) and time of exposure. The toxic effect was not prevented by serum factors nor by bovine serum albumin. Fluorescein-conjugated phalloidin was used to examine the arrangement of actin filaments at substrate adhesion regions and cell-cell contacts. Primary events following exposure to tacrine included changes in cell morphology, disappearance of actin filament bundles, and disruption of focal adhesion contacts. At concentrations between 10 and 50 microM, tacrine induced neurite outgrowth in Neuro 2A cells, an effect that was not observed in B12 cells, suggesting that certain tacrine effects could be specific for neuronal cells. Although similar trends of response were observed for both cell types, some differences between undifferentiated and differentiated cells were apparent.
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PMID:Responses induced by tacrine in neuronal and non-neuronal cell lines. 958 88

Acetylcholinesterase (AChE), the enzyme involved in the hydrolysis of the neurotransmitter acetylcholine, has been implicated in non-cholinergic actions which may play a role in neurodegenerative diseases such as Alzheimer's disease. To study the potential cytotoxicity of brain AChE, the effects of affinity purified AChE were analyzed on neuronal (Neuro 2a) and glial-like (B12) cells. LDH release and MTT reduction assays showed that AChE was toxic; the toxicity was dependent on the enzyme concentration, time of incubation and cellular density. The toxic effect of AChE was not related to its catalytic activity, since the anti-cholinesterase drug BW284C51 and heat inactivation were unable to block the effects of the enzyme. When cells were incubated at 4 degrees C, toxicity was completely blocked, in contrast to cells incubated at 37 degrees C. The presence of serum in the culture medium inhibited the toxic effects of AChE. Cytoplasmic shrinkage, condensation and fragmentation of nucleus as well as DNA strand breaks detected with the TUNEL technique indicated that apoptotic cell death is involved in the effect of AChE. Considering that we have previously shown that AChE promotes the assembly of beta-amyloid peptide into neurotoxic amyloid fibrils, it is conceivable that the neurotoxicity of AChE shown here may play a role in the neuronal degeneration observed in Alzheimer's disease.
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PMID:Toxic effects of acetylcholinesterase on neuronal and glial-like cells in vitro. 967

The pathophysiology of Alzheimer's disease is complex and involves several different biochemical pathways. These include defective beta-amyloid (Abeta) protein metabolism, abnormalities of glutamatergic, adrenergic, serotonergic and dopaminergic neurotransmission, and the potential involvement of inflammatory, oxidative and hormonal pathways. Consequently, these pathways are all potential targets for Alzheimer's disease treatment and prevention strategies. Currently, the mainstay treatments for Alzheimer's disease are the cholinesterase inhibitors, which increase the availability of acetylcholine at cholinergic synapses. Since the cholinesterase inhibitors confer only modest benefits, additional non-cholinergic Alzheimer's disease therapies are urgently needed. Several non-cholinergic agents are currently under development for the treatment and/or prevention of Alzheimer's disease. These include anti-amyloid strategies (e.g. immunisation, aggregation inhibitors, secretase inhibitors), transition metal chelators (e.g. clioquinol), growth factors, hormones (e.g. estradiol), herbs (e.g. Ginkgo biloba), nonsteroidal anti-inflammatory drugs (NSAIDs, e.g. indomethacin), antioxidants, lipid-lowering agents, antihypertensives, selective phosphodiesterase inhibitors, vitamins (E, B12, B6, folic acid) and agents that target neurotransmitter or neuropeptide alterations. Neurotransmitter receptor-based approaches include agents that modulate certain receptors (e.g. nicotinic, muscarinic, alpha-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid [AMPA], gamma-aminobutyric acid [GABA], N-methyl-D-aspartate [NMDA]) and agents that increase the availability of neurotransmitters (e.g. noradrenergic reuptake inhibitors). Of these strategies, the NMDA receptor antagonist memantine is in the most advanced stage of development in the US and is already approved in Europe as the first treatment for moderately severe to severe Alzheimer's disease. Memantine is proposed to counteract cellular damage due to pathological activation of NMDA receptors by glutamate. Results with Ginkgo biloba have been mixed. Data for neurotrophic therapies and vitamin E (tocopherol) appear promising but require confirmation. NSAIDs and conjugated estrogens have not proven to be of value to date for the treatment of Alzheimer's disease. Statins may have a potential role in reducing the risk or delaying the onset of Alzheimer's disease, although this has yet to be confirmed in randomised trials. There are currently no data to support the use of statins as a treatment for dementia. This article provides an update on the current status of selected agents, focusing primarily on those agents with the most extensive clinical evidence at present.
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PMID:Non-cholinergic strategies for treating and preventing Alzheimer's disease. 1242 Nov 15

The British Association for Psychopharmacology (BAP) coordinated a meeting of experts to review the evidence on the drug treatment for dementia. The level of evidence (types) was rated using a standard system: Types 1a and 1b (evidence from meta-analysis of randomised controlled trials or at least one controlled trial respectively); types 2a and 2b (one well-designed study or one other type of quasi experimental study respectively); type 3 (non-experimental descriptive studies); and type 4 (expert opinion). There is type 1a evidence for cholinesterase inhibitors (donepezil, rivastigmine and galantamine) for mild to moderate Alzheimer's disease; memantine for moderate to severe Alzheimer's disease; and for the use of bright light therapy and aromatherapy. There is type 1a evidence of no effect of anti inflammatory drugs or statins. There is conflicting evidence regarding oestrogens, with type 2a evidence of a protective effect of oestrogens but 1b evidence of a harmful effect. Type 1a evidence for any effect of B12 and folate will be forthcoming when current trials report. There is type 1b evidence for gingko biloba in producing a modest benefit of cognitive function; cholinesterase inhibitors for the treatment of people with Lewy body disease (particularly neuropsychiatric symptoms); cholinesterase inhibitors and memantine in treatment cognitive impairment associated with vascular dementia; and the effect of metal collating agents (although these should not be prescribed until more data on safety and efficacy are available). There is type 1b evidence to show that neither cholinesterase inhibitors nor vitamin E reduce the risk of developing Alzheimer's disease in people with mild cognitive impairment; and there is no evidence that there is any intervention that can prevent the onset of dementia. There is type 1b evidence for the beneficial effects of adding memantine to cholinesterase inhibitors, and type 2b evidence of positive switching outcomes from one cholinesterase inhibitor to another. There is type 2a evidence for a positive effect of reminiscence therapy, and type 2a evidence that cognitive training does not work. There is type 3 evidence to support the use of psychological interventions in dementia. There is type 2 evidence that a clinical diagnosis of dementia can be made accurately and that brain imaging increases that accuracy. Although the consensus statement dealt largely with medication, the role of dementia care in secondary services (geriatric medicine and old age psychiatry) and primary care, along with health economics, was discussed. There is ample evidence that there are effective treatments for people with dementia, and Alzheimer's disease in particular. Patients, their carers, and clinicians deserve to be optimistic in a field which often attracts therapeutic nihilism.
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PMID:Clinical practice with anti-dementia drugs: a consensus statement from British Association for Psychopharmacology. 1706 Mar 46

Cognitive speed, inhibitory function, and memory decline with age while crystallised, particularly verbal, abilities remain largely intact. Poor health, fewer years of education, lower activity, the presence of the APOE E4 allele, and high BP appear to predict faster cognitive decline. Dementia is diagnosed in the presence of objective cognitive impairment, both long- and short-term memory, plus at least one additional (cortical) cognitive deficit, such as dysphasia, dyspraxia, agnosia, or disturbance in executive functioning. In addition, patients have to show significant impairment in social or occupational functioning and a significant decline from previous levels. Both smoking and diabetes increase the risk of all types of dementia, not smoking or even stopping smoking reduces this risk, but better control of type 2 diabetes does not appear to have a measurable effect. Drinking small to moderate amounts of alcohol appears to confer some benefit in ameliorating cognitive decline. There is some evidence that HRT, DHEA, BP lowering in patients without prior cerebrovascular disease, statins, vitamin B6 and procaine are NOT helpful. There is insufficient evidence to establish or refute a beneficial effect for exercise, treatment of type 2 diabetes, omega-3 fatty acids, folic acid with/without vitamin B12, antioxidant vitamins, or ginkgo biloba. Depressive symptoms are more prevalent than dementia. Clinical (major) depression can present with cognitive deterioration, often associated with subjective complaints. Patients with subjective or objective memory impairment, but without functional deterioration, can be referred to the local memory clinic, while demented patients eligible for acetylcholinesterase inhibitor treatment, patients whose diagnosis is unclear and who may need some specific investigations, as well as patients who may benefit from a combined approach with psychotropic drugs and behavioural support should be referred to the local mental health team.
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PMID:Normal cognitive decline or dementia? 2019 32


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