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 lungs of rat fetuses at various stages of gestation and lungs of infant rats were examined histochemically for acetylcholinesterase (AChE) and norepinephrine (NE). No AChE is present in the fetal lungs until 15 days of gestation. At this stage a number of large round cells appear which stain heavily for AChE. These cells disappear by the 18th day of development and at 18 days no AChE-positive structures are demonstrable within the lung. The large AChE-positive cells are of similar size and distribution to fluorescent cells which become apparent after treatment of the mothers with L-DOPA. At 20 days, the day before delivery, a diffuse AChE reaction appears in the walls of large branches of intrapulmonary bronchi. At 20 days, also, sparse NE-containing nerves are present near the hilum and extend along bronchial arteries into the lung. Not until birth do AChE-containing nerves appear in intrathoracic structures. These are vagal preganglionic and postganglionic fibers near the trachea, bronchi, and esophagus. AChE-positive ganglion cells are present in the walls of extrapulmonary bronchi at birth, and perimuscular nerve plexuses containing AChE are also present in the bronchial walls. NE-containing nerves are visible in several divisions of the bronchial artery at birth. Three days postnatally, AChE-containing nerves have not yet invaded intrapulmonary structures, but at this stage the adult pattern of adrenergic innervation is present. By the fifth postnatal day, sparse AChE-positive nerves are associated with intrapulmonary bronchi, and rats 9 days old present the adult pattern of cholinesterase-containing nerves.
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PMID:Acetylcholinesterase- and norepinephrine- containing nerves in developing rat lung. 74 48

The dermal cells in grey, xanthic, and white goldfish integuments were cytochemically characterized for the following enzymatic activities: tyrosinase, DOPA-oxidase, cytochrome oxidase, monoamine oxidase, peroxidase, non-specific esterase, cholinesterase, NAD-diaphorase, NADP-diaphorase, aryl sulfatase, nucleotide phosphodiesterase, beta-glucuronidase, acid phosphatase, alkaline phosphatase, adenosine triphosphatase, thiamine pyrophosphatase, glucose-6-phosphatase, aldolase, as well as succinate, malate, isocitrate, glutamate, glucose-6-phosphate, 6-phosphogluconate, alpha-glycerophosphate, alcohol, lactate, and beta-hydroxybutyrate dehydrogenases. It was found that the epidermis was a significant barrier to the access of cytochemical reaction substrates. Removal of the epidermal barrier provided dermal cell localizations of enzymatic activities which were reproducible. Further, alterations in reaction times and temperatures from the mammalian methodology provided conditions fe various integumental cells were compared for possible interrelationships. The basic foundations for future work with the dermis of poikilothermic vertebrates on an experimental basis were established. In addition, a previously undescribed non-pigmented dermal cell, the "x"-cell, was found to have enzymatic characteristics similar to both melanophores and lipophores. The "x"-cell may be the common precursor of both types of pigment cells.
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PMID:Cytochemical characterization of goldfish (Carassius auratus L.) dermis with special reference to the pigment cells. 82 86

It has been revealed by the open field tests that Wistar male rats with a high motor activity exhibit elevated emotional reactivity and sensitivity to small doses of L-DOPA. This rat group was examined for acetylcholine (AC) metabolism according to choline acetyltransferase (CAT) and acetyl cholinesterase (ACE) activity in fractions of light (C) and heavy (D) synaptosomes of the hypothalamus and nucleus of the solitary tract (NST) in health and after three-fold administration of L-DOPA. In health, the D fraction of the NST demonstrated "non-classic" high activity of both enzymes. In view of this fact it may be assumed that terminals of the fibers of craniocerebral nerves IX and X are localized in that fraction. In the NST, L-DOPA produces a decrease of CAT and ACE activity and of protein content in the D fraction, which corresponds with inhibition of the function of the parasympathetic (AC-ergic) system in response to activation of the peripheral adrenergic system. In the C fraction of the NST, the analogous but opposiely directed changes are observable, which may be related to compensation of the peripheral effect produced by L-DOPA. In turn, the C and D fractions of hypothalamic synaptosomes manifest noticeable activation of ACE, with CAT activity and protein content being unchanged. In contrast to the NST, this phenomenon is not connected with the changes in the rate of AC synthesis. Therefore, the status of the AC system of hypothalamic synaptosomes does not correlate with its possible appearance on the NST and is thus not related to participation of the hypothalamus in regulation of vegetative functions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Biochemical aspects of the pathogenesis of autonomic and emotional disorders in functional disorders of the dopamine system]. 166 9

The specific binding of the agonists [3H]clonidine and [3H]UK 14304 (bromoxidine) and of the antagonist [3H]RX 821002 (2-metoxy idazoxan) to rat brain membranes, as well as clonidine-induced mydriasis, clonidine-induced inhibition of brain (3,4-dihydroxyphenylalaninme) DOPA synthesis and clonidine-induced inhibition of twitch responses in the vas deferens, was used to evaluate the density and sensitivity of central and peripheral alpha 2-adrenoceptors after prolonged activation of the cholinergic system. Acute (12 h), short-term (4 days) or chronic (7-18 days) treatment with the cholinesterase inhibitors neostigmine (0.1 mg/kg), physostigmine (0.1 mg/kg) and diisopropylfluorophosphate (2 mg/kg) and with the muscarinic receptor agonist pilocarpine (10 mg/kg) did not alter the density of brain alpha 2-adrenoceptors. In contrast, various functional responses mediated by central and peripheral alpha 2-adrenoceptors were potentiated after the repeated treatments. Thus, the inhibitory alpha 2-autoreceptor that modulates the synthesis of brain noradrenaline and the central postsynaptic inhibitory alpha 2-adrenoceptor that induces mydriasis displayed greater responses in vivo after chronic treatment with neostigmine or pilocarpine. These treatments also increased the sensitivity of peripheral presynaptic alpha 2-adrenoceptors in the vas deferens. The results indicate that prolonged activation of central and peripheral cholinergic pathways results in up-regulation of alpha 2-adrenoceptor function without apparent increases in receptor density.
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PMID:Acute and chronic effects of cholinesterase inhibitors and pilocarpine on the density and sensitivity of central and peripheral alpha 2-adrenoceptors. 810 72

Peculiarities of the CNS response to chronic treatment with L-DOPA were revealed by quantitative cytochemical methods in August (stress-sensitive) and Wistar (emotionally resistant) rats. In August rats L-DOPA administration caused aminopeptidase activity increase in sensomotor cortex layer 3 and nucleus accumbens, glutamate dehydrogenase activity growth in nucleus accumbens as well as the elevation of monoaminoxidase (MAO) activity in nucleus caudatus and nucleus accumbens (serotonin as substrate) and in nucleus caudatus and hippocampus (tryptamine as substrate), while acetyl cholinesterase activity did not change at all. At the same time in Wistar rats only glutamate dehydrogenase activity increase was observed in nucleus caudatus and nucleus accumbens.
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PMID:[Comparative cytochemical study of the central nervous system in Wistar and August rats in dopamine system hyperfunction]. 960 63

The syndrome of dementia with Lewy bodies (DLB) is characterised by the clinical triad of fluctuating cognitive impairment, recurrent visual hallucinations and spontaneous motor features of Parkinsonism. In an attempt to define DLB as a distinct clinical syndrome separate from Alzheimer's disease (AD) and Parkinson's disease (PD) with dementia, a consensus workshop in 1995 established a new set of diagnostic criteria. Dementia that precedes or accompanies the onset of spontaneous (i.e., not neuroleptic-induced) Parkinsonism is termed DLB. In addition, fluctuations in alertness, cognition and function and visual hallucinations are emphasised and included as core features of DLB. The degree to which an individual patient exhibits cognitive impairment, behavioural problems and Parkinsonian features is variable. Therefore, treatment must be individualised. Although there are no officially approved drugs for DLB, limited experience from clinical trials, as well as past experience with the treatment of AD and PD patients, provide some basis for making drug choices. The cholinergic deficit seen in DLB makes cholinesterase inhibitor drugs the mainstay of treatment for cognitive impairment. This class of drugs has also shown therapeutic benefit in reducing hallucinations and other neuropsychiatric symptoms of the disease. Because of their relatively greater therapeutic window, cholinesterase inhibitors are also used as first-line therapy for the treatment of psychosis in DLB. Patients with DLB are extremely sensitive to the extrapyramidal side effects of neuroleptic medications. Thus, only atypical antipsychotic agents such as quetiapine, should be considered as alternative treatment for psychosis. Anxiety and depression are best treated with selective serotonin re-uptake inhibitors, whereas REM sleep behaviour disorder may be treated with low dose clonazepam. Parkinsonism responds to dopaminergic agents; however, precipitation or aggravation of hallucinosis may occur. Levodopa is preferred over dopamine agonists due to its lower propensity to cause hallucinations and somnolence. As the diagnostic criteria for DLB become more refined and validated by postmortem studies, it is hoped that rigorous, well-designed trials will be performed, aimed at alleviating the primary target symptoms of dementia, psychosis and Parkinsonism.
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PMID:Pharmacotherapy of dementia with Lewy bodies. 1459 56

Neurodegenerative disorders result from premature progressive degeneration of specific neurons, and manifest as diseases or syndromes with varied combinations of cognitive, motor, sensory and autonomic dysfunctions. The management involves pharmacotherapy as well as non-pharmacological measures and also to lessen the burden of the care-givers. The medications available for medical treatment are: Levodopa, dopamine agonists, amantadine, anticholinergics, enzyme inhibitors, etc. Advanced Parkinson's disease is concerned with management of motor complications and non-motor complications. Recently surgical treatment is a great option for managing motor complication. Orthostatic hypotension, gait distiurbances, emotional and psychiatric problems, sleep disturbances can be managed and had been discussed in brief. Currently there is no medication available for the cure of Alzheimer's disease. The specific medications claimed to improve patient's well being and cognition include cholinesterase inhibitors, N-methyl-D-aspartate receptor antagonist, anti-oxidants, and anti-amyloid therapy. While medical and surgical treatments for Parkinson's disease have revolutionised the management, still drug therapy for Alzheimer's disease is dismal.
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PMID:Management of neurodegenerative disorders: Parkinson's disease and Alzheimer's disease. 1617 94

Gait disorders form part of the axial symptoms observed in Parkinson's disease (PD) and also represent a major source of therapeutic failure in the later stages of PD, with the appearance of freezing of gait (FOG) and falls. Double-blind clinical trials and, above all, clinical experience have demonstrated that l-DOPA is effective in reducing FOG. Dopaminergic agonists appear to be less effective than l-DOPA and lack formal proof of their efficacy. The enzyme inhibitors provide modest benefits, which need to be confirmed. Hence, these symptoms appear to be partially doparesistant and justify investigation of other major neurotransmission systems. Of the various drugs with partial noradrenergic activity, methylphenidate may improve FOG and attention disorders. Memantine has shown some value in improving motor symptoms and gait in fluctuating parkinsonian patients - possibly by reducing the effect of glutamatergic hyperactivation of the subthalamic nucleus on the pedunculopontine nucleus (PPN). The PPN's dense cholinergic innervation also suggests that cholinesterase inhibitors may be of use, although any benefits must be set against a potential aggravation of rest tremor. The many interactions between the serotoninergic and dopaminergic systems require the implementation of clinical studies on the complex motor impact of serotoninergic treatments, which may aggravate the parkinsonian syndrome while improving gait (as is the case with paroxetine and ritanserin). This review seeks to develop the various pathophysiological hypotheses prompted by the results of fundamental studies and pilot clinical trials, with a view to justifying the implementation of confirmatory, double-blind, placebo-controlled therapeutic trials.
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PMID:[Pharmacological hypotheses and therapeutic strategies for gait disorders in Parkinson's disease]. 1981 97

Patients with Parkinson's disease (PD) have a high risk of psychiatric complications, like depressive or psychotic syndromes, dementia and sleep disorders. Although these disorders may even precede the onset of motor symptoms, they are often not recognized and therefore not adequately treated. This article provides a comprehensive overview of the therapeutic options of the most commonly observed psychopathological syndromes in PD. In the case of depressive syndromes medication could be optimized by making use of dopamine agonists that have been proven to have antidepressant properties. In recent studies tricyclic antidepressants showed stronger effects than SSRI. Psychotic symptoms are most often evoked by dopaminergic therapy or are seen in the course of cognitive decline. The therapeutic regimen should be built mainly on L-Dopa medication in the lowest tolerated dose, if required in combinations with COMT-Inhibitors. When antipsychotic medication is indicated, clozapine is the first choice. Quetiapine might also be useful in many patients. Psychotic symptoms in demented patients may respond to cholinesterase-inhibitors, that also delay cognitive decline. Patients with PD require an individually optimized therapeutic regimen not only for motor symptoms, but also for frequently occurring psychiatric syndromes since these strongly influence the patients' and their caregivers' quality of life, are predictors for hospitalization and therefore have great economic importance for health care systems.
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PMID:[Treatment of mental disorders in patients with Parkinson's disease]. 2042 92

Dementia with Lewy-bodies (DLB) and Parkinson's disease dementia (PDD) are no rare causes of dementia. Both have neuropathologically, clinically, and neurochemically much in common. In the course of both conditions frequently psychotic symptoms occur, often induced by antiparkinsonian medication. Treatment of psychotic features with conventional antipsychotics is not tolerated in many cases. Therefore low-dose clozapine treatment is acknowledged usual practise for psychosis in Parkinson's disease and a case report indicates efficacy for psychosis in DLB, too. All other atypical antipsychotics except risperidone are not licensed for dementia in Germany, but risperidone is contraindicated in DLB due to manufacturer's notice and usually not well tolerated in DLB and Parkinson's disease. Open trials indicate safety for treatment of psychosis in DLB and PDD with quetiapine. Randomized controlled trials indicate, that quetiapine is less effective than clozapine against psychotic symptoms in both conditions, although comparatively safe. Cholinesterase inhibitors, especially rivastigmine, are a therapeutic alternative for treating both psychotic and cognitive symptoms in both conditions. Parkinsonism in DLB-patients responds worse to levodopa compared to patient with Parkinson's disease. Anticholinergic drugs often induce delirium in demented patients and therefore should be avoided. The same problem is associated with dopamine agonists in PDD and DLB. Amantadine, a NMDA-receptor antagonist like memantine, potentially bears the same risk of worsening psychotic symptoms. The following preliminary recommendation for drug treatment of PDD and DLB can be given: Stop all anticholinergic medication and reduce levodopa and other antiparkinsonian medication to the tolerated minimum. Levodopa alone is preferred. Treat with cholinesterase inhibitors to the maximum tolerated dose. If there is no adequate response regarding psychotic symptoms, add quetiapine. If this approach fails, replace quetiapine by low-dose clozapine. If behavioural disturbances are due to depression, anxiety, or irritability, treatment with an antidepressant, preferably citalopram, is an option.
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PMID:[Drug treatment of dementia with Lewy bodies and Parkinson's disease dementia--common features and differences]. 2142 15


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