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)

An analysis of the respiratory function of workers of a chemical factory producing Enolophos was carried out. All workers were included in the study-41 men (age range 23-59 years, mean working duration 4.9 years). In 48.8% chronic bronchitis was diagnosed. Spirometric analysis was carried out using an electronical spirometer with a steady volume plethysmograph. The following along with other pulmonary mechanics parameters were assessed: compliance, airway resistance. An increase of the FEV1%VC index was seen in 34.2% and RV/TLC in 40%. Compliance was increased in 30%. Airway resistance was increased especially in subjects with chronic bronchitis and a decrease in FEV1, FEV1%VC, FEF50, FEF25 rates. In patients with decreased erythrocyte acetylcholinesterase activity only increased airway resistance was seen. The duration of working in this factory did not affect respiratory function. The results demonstrate a harmful effect of Enolophos to the lungs and airways.
Pneumonol Pol
PMID:[Evaluation of respiratory tract function in workers employed in the production of Enolophos]. 861 65

Paraneoplastic Lambert-Eaton myasthenia syndrome is presented in two cases with small cell lung cancer. An increase of serum cholinesterase activity was explained by induced release of biologically active proteins by neoplastic tissue.
Pol Merkur Lekarski 1997 Feb
PMID:[Two cases of Lambert-Eaton syndrome with an increase of serum cholinesterase activity]. 953 60

The costs of Alzheimer's disease treatment in the era of acetylcholinesterase inhibitors use are critically discussed.
Psychiatr Pol
PMID:[The costs of Alzheimer's disease treatment: the rationale of acetylcholinesterase inhibitors use?]. 1076 41

In 1983, we reported that intracerebral or systemic administration of cholinergic agents produced seizures and seizure-related brain damage in rodents. During the following 17 years, seizures induced by cholinomimetic drugs became a popular model of epilepsy. Seizures can by produced by cholinergic agonists acting directly at muscarinic receptors or by drugs enhancing cholinergic transmission due to the inhibition of acetylcholinesterase activity. Status epilepticus evoked by pilocarpine in rodents triggers long-lasting changes which can be described as: (I) acute-onset seizures lasting for several hours, (II) a silent period characterized by normalization of electroencephalographic patterns lasting for days, and (III) spontaneous recurrent seizures lasting for life. Therefore, seizures induced by cholinomimetics in rodents are of value for studies of basic mechanisms of epileptogenesis and action of antiepileptic drugs.
Pol J Pharmacol
PMID:Pilocarpine-induced seizures in rodents--17 years on. 1094 24

Alzheimer's disease is the most common cause of memory disruption in elderly people. The main pathogenic factor of the disease is beta-amyloid protein, which may cause toxic damage of neurones. Other suggested pathogenic factors include an inflammatory process around the senile plaques, apoptosis and necrotic death of neurones, and, in consequence, changes in functioning of neurotransmitter systems. In this article the authors present the main directions in pharmacotherapy of Alzheimer's disease: causal therapy, which prevents the neurodegenerative changes and slows down the pathogenetic process, and symptomatic therapy. The aim of symptomatic therapy is to reduce memory disruption and psychiatric symptoms associated with the disease. Positive influence on cognitive processes is exerted by cholinergic drugs, e.g. the actually used inhibitors of acetylcholinesterase (rivastigmine, donepezil), the nootropic agents (piracetam, nefiracetam) and extracts of Gingko biloba. For treatment of the disease accompanying psychiatric symptoms (anxiety, depression, hallucinations, sleepness) the drugs with minimal influence on cognitive processes are recommended. Attempts at causal therapy are focussed on searching for the substances that can prevent the formation and toxicity of beta-amyloid (droloksifen, estrogens, agonists of muscarinic receptors M1), the cytotoxic influence of excitatory aminoacids (memantine, lamotrigine), calcium (nimodipine) and free radicals (selegiline, alpha-tocoferol), and the development of inflammatory process (non-steroidal antiinflammatory drugs). The new target of research is correction of deficits of nerve growth factor and neurotransmitters by intracerebral implantation of modified fibroblasts. Another way is prevention of the formation of amyloid plaques using appropriate antisense oligonucleotides.
Psychiatr Pol
PMID:[Perspectives of therapy of Alzheimer's disease]. 1105 61

Behavioural disturbances are common in the course of dementia in Alzheimer's disease (AD) and their treatment is usually difficult. Different pharmacological and non-pharmacological options are employed basing mainly on clinical experience, still the number of well-designed, controlled studies in the field is very small. Novel, atypical neuroleptics, including risperidone might potentially be one of these options, taking into account their good safety profile and clinical efficacy in closely related syndromes. We present the results of a retrospective analysis of 57 outpatients with behavioural symptoms complicating AD treated with risperidone, either alone or in combination with one of the acetylcholinesterase inhibitor (AchEI; donepezil or rivastigmine). Seventy five percent of patients treated responded to risperidone with the usual effective dose of 0.5-1 mg/day. The influence of risperidone treatment on behavioural symptomatology was irrespective to the use of AchEI and equally well safe in both groups. The clinical response to the treatment was seen usually within first 2-3 weeks, those who did not respond early tended not to respond later on as well. Additionally, if not responding to low doses of risperidone (0.5-1 mg/day), patients usually did not respond to higher doses or could not tolerate them, mainly due to emerging extrapyramidal symptoms (EPS). Low doses of risperidone were well tolerated, with the fraction of patients experiencing EPS not achieving 10%. EPS observed, were dose dependent and tended to appear if the dose acceleration was fast. We then recommend low doses of risperidone and its slow titration if needed.
Psychiatr Pol
PMID:[Risperidone in the ambulatory treatment of behavior disorders in demented patients of Alzheimer's type: a retrospective analysis]. 1187 83

Centrally acting cholinesterase inhibitors (ChEls) improve cognitive functions in Alzheimer's disease (AD) and other forms of dementia. Evaluation of treatment efficacy is based mainly on subjective assessment tools which includes standardized neuropsychological tests. Therefore, an additional objective tool for the evaluation of drug response is necessary. Thirty two patients were treated with ChEls for dementia (tacrine 19, donepezil 5, rivastigmine 8). Cognitive response was assessed before ChEls (baseline) and after 26 weeks, as optimal tolerated doses were achieved and maintained (endpoint). Evaluation included repeated measurements of Mini Mental State Examination (MMSE), ADAS-cog and P300. For statistical analysis we used ANOVA with repeated measures and Pearson correlation coefficient. Results demonstrated improvement of mean ADAS-cog by 2.0 points (from 29.4 to 27.4 p = 0.08) while MMSE remained almost unchanged (20.1 to 19.8). Mean P300 latency reduced significantly by 24 msec (from 383 msec to 359 msec, p = 0.0001) thus reflecting the clinical improvement. However mean amplitudes did not change from baseline to endpoint (13 microvolts). Significant correlation was found between mean ADAS-cog and mean P300 latency at baseline and end-point (R = 0.452 p = 0.014, R = 0.567 p = 0.001 respectively). Strong correlation was found between mean MMSE and P300 latency at Baseline (R = -0.335 p = 0.07), and significant correlation was found at endpoint (R = -0.613 p < 0.001). Our data suggests that P300 is a reliable instrument for assessment of cognitive response to ChEls in demented patients.
Neurol Neurochir Pol 2001
PMID:Evaluation of cholinergic treatment in demented patients by P300 evoked related potentials. 1200 52

This paper reviews treatment strategies of myasthenia gravis (MG) that are currently in use: 1. enhancement of neuromuscular transmission with acetylcholinesterase inhibitors; 2. short-term immunotherapies, including plasma exchange and intravenous immunoglobulin therapy; 3. immunosuppression; 4. surgical thymectomy and thymomectomy. Acetylcholinesterase blockers are still used as the first-line treatment of MG. Although most of patients benefit from these drugs, the improvement is usually incomplete and often wanes after weeks or months of treatment. When clinical symptoms are not adequately controlled by anticholinesterase drugs, immunosuppressive therapy is suggested, but indications for treatment take into account age and clinical symptoms (ocular versus generalised myasthenia). Steroids are the most commonly used and most consistently effective immunosuppressive agents for MG treatment but they also have the highest incidence of potential side effects. The use of azathioprine, for monotherapy in initial immunosuppression treatment of MG is controversial. However, data are available, including a randomised trial, to support the use of azathioprine as an adjunctive drug with corticosteroids. Retrospective analyses of the treatment of MG have shown that cyclosporine is also effective but renal toxicity and hypertension are the major factors limiting its use. Mycophenolate mofetil appeared also to be effective as adjunctive therapy in the treatment of refractory and steroid-dependent MG. Intravenous immunotherapy (IVIg) is recommended as an adjunct in the management of MG exacerbations. According to new publications, there are no pronounced differences in the efficacy of IVIg treatment and plasma exchange. Thymomectomy is beneficial and should be considered for all patients with thymoma-associated MG. However, in cases with non-thymomatous autoimmune MG, thymectomy is recommended only for patients below age 55-60 and within the first 6-12 months of disease duration.
Pol Merkur Lekarski 2003 Mar
PMID:[Actual aspects of myasthenia gravis treatment]. 1291 9

Memantine is an NMDA receptor antagonist with moderate affinity, which results in neuroprotective potential due to reducing overstimulation caused by glutamate (excitotoxicity) and simultaneous lack of adverse events (especially psychosis) typical for an antagonist with higher affinity like phencyclidine. In randomized, controlled studies it has been shown that memantine is beneficial in the treatment of moderate to severe dementia of Alzheimer's type and it became the very first compound to be registered for this purpose both in Europe (including Poland) and in the United States. Further investigation require usefulness of memantine in less advanced stages of Alzheimer's disease as well as other types of dementia especially vascular; promising results are shown in dual therapy: memantine + cholinesterase inhibitor.
Psychiatr Pol
PMID:[The clinical relevance of memantine use]. 1530 96

In a search for new acetylcholinesterase (AChE) inhibitors, derivatives of N-alkyl carbamates of a-substituted N-benzylamides of g-hydroxybutyric acid (GHB) 2(a-d); 3(a-d); 4(a-d) were obtained. Starting from 3-bromo-tetrahydrofuran-2-one, and N-phenylpiperazine 3-(4-phenylpiperazin-1-yl) tetrahydrofuran-2-one (1) was obtained. The aminolysis of lactone 1 with 4-substituted derivatives of benzylamine yielded N-substituted benzylamides of a-(4-phenylpiperazin-1-yl)-g-hydroxy-butyric acid (2-4). The target compounds were prepared by refluxing N-substituted benzyl-amides of a-(4-phenylpiperazinyl-1-)-GHB with ethyl-, i-propyl-, n-propyl- or n-butyl-isocyanate in dry acetonitrile. The inhibitory potency of AChE was evaluated by means of Ellman's in vitro test.
Acta Pol Pharm 2004 Dec
PMID:Synthesis of novel N-alkyl carbamates of a-substituted amides of g-hydroxybutyric acid as potential acetylcholinesterase inhibitors. 1590 54


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