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)

Pathological changes of the fusimotor endings in parkinsonism, motor neuron disease and myasthenia were examined by the acetylcholinesterase technic on serial sections. In parkinsonism, the diffuse endings, which are thought to be supplied by the static gamma nerve fibers, showed remarkable enlargement, while en plaque and en grappe endings were atrophic. In motor neuron disease, en plaque and en grappe endings, which are thought to be innervated by the beta nerve fibers and dynamic gamma nerve fibers respectively, revealed marked atrophy. However the diffuse endings were normal. In myasthenia gravis and myasthenic syndrome (Eaton-Lambert syndrome), en plaque and en grappe endings were atrophic, though only the diffuse endings were spared. The significance of these changes in the fusimotor endings is discussed.
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PMID:Histochemical study of the muscle spindles in parkinsonism, motor neuron disease and myasthenia. An examination of the pathological fusimotor endings by the acetylcholinesterase technic. 8 59

Over the period November 1978 to October 1988, 46 cases of motor neuron disease were seen at Kenyatta National Hospital, Nairobi. One case was seen in private practice. A bimodal age distribution of the disease was identified with a peak in the fourth decade of life and another peak in the sixth decade of life. The disease seen in the fourth decade of life was different as seen in other parts of the world in that the majority of patients tended to present with very rapidly progressive disease despite the primary presentation with limb symptoms and signs. Serum cholinesterase activity in five of these patients and five of the classical motor neuron disease revealed no abnormalities. This unusually rapidly progressive disease in young adults has not been described anywhere. The disease seen in older age groups and especially in patients over fifty years of age was not different from the one seen in other parts of the world.
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PMID:Unusual form of motor neuron disease in Kenya. 150 87

Conditions have been developed for the culture of rat spinal cord neurons in serum-free media supplemented with hormones and growth factors. Neurons were identified by immunofluorescence-labeled anti-neurofilament antibody, and their growth was monitored by assay of choline acetyltransferase and cholinesterase activities. Activities of these enzymes were considerably higher than those of comparable cultures in serum supplemented media in which there were visibly many more nonneuronal cells. Serum immunoglobulins from patients with motor neuron disease showed enhanced binding to rat spinal cord cells maintained in both serum-supplemented and serum-free media, as compared with those from normal healthy individuals. Enhanced binding was more marked with the latter cells, presumably because of the higher proportion of neuronal cells in these cultures. Serum immunoglobulins from patients with other neurologic disorders showed a similar binding to that of the normal controls. The results demonstrate the presence of an immune response to spinal cord cell membrane components in patients with motor neuron disease, although whether the response is primary or secondary in the disease process remains unclear.
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PMID:Cultured rat spinal cord neurons: interaction with motor neuron disease immunoglobulins. 404 91

Acetylcholinesterase (AChE) activity was measured in the presence of the specific inhibitor of pseudocholinesterase, iso-OMPA, in plasma from patients with amyotrophic lateral sclerosis (ALS), progressive muscular atrophy (PMA), neuromuscular disease controls, and normal controls. Both AChE and Na-K ATPase activities were measured in erythrocyte ghost membranes from ALS and normal controls. Activities of erythrocyte ghost AChE and Na-K ATPase did not differ between ALS and control patients, suggesting that erythrocyte membranes were normal in ALS. However, the activity of plasma AChE in patients with ALS and PMA was increased significantly over plasma activity in disease controls and normal controls. In addition, in an animal model of human PMA, the Wobbler mouse, plasma AChE activity was increased significantly over littermate controls. The explanation for the increase in plasma acetylcholinesterase was not clear; however, a number of potentially useful clinical points followed from this study. First, there was no relationship between a specific subtype of motor neuron disease and the level of AChE activity. Second, AChE activity appeared to vary directly with the duration of PMA but not with the severity of PMA. This did not correlate with either the duration or severity of ALS. Last, plasma AChE activity was normal in about 30% of patients who had motor neuron disease; therefore, AChE assay had limited use in the diagnosis of ALS or PMA.
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PMID:Acetylcholinesterase and ATPases in motor neuron degenerative diseases. 613 69

An hypothesis regarding the pathogenesis of amyotrophic lateral sclerosis is presented, which places emphasis on extraneural cells. Classical experimental denervation is compared and contrasted with motor neuron disease, both from information in the literature as well as concepts deriving from the hypothesis. Background information regarding neuromuscular junction-specific (16S) acetylcholinesterase and a basal lamina-enriched surface glycoprotein (fibronectin) are presented, which suggest not only their mutual interaction, but likely parallel regulation on muscle cell surfaces by the motor nerve. Since 16S acetylcholinesterase likely contains basal lamina-type collagen and fibronectin specifically associates with collagen, a model relating activation of latent collagenase enzyme in amyotrophic lateral sclerosis is described. It is suggested that continued degeneration, including transneuronal effects, of the motor system ensues from random, continuous loss of nerve-muscle adherence resulting from collagen resorption at the neuromuscular junction.
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PMID:Neuromuscular junction macromolecules in the pathogenesis of amyotrophic leteral sclerosis. 624 44

Regional distribution of enzymic activities in acetylcholine (ACh) metabolism was examined on thinly-sectioned transverse slices of human spinal cords obtained during autopsy of 5 motor neuron disease (MND) and 5 control patients without MND. Choline acetyltransferase (ChAT) activity was highly concentrated in the ventral horn regions (gray and white matters) of cervical, thoracic and lumbar spinal cord of non-MND patients. This enzyme activity was found to be remarkably low in the ventral gray and white matter of MND patients compared with that of the controls. Although the distribution of acetylcholinesterase (AChE) activity was found to be high in both ventral and dorsal gray matter of the spinal cord, little difference was observed between each corresponding region of MND and control patients, except relatively low enzyme activity in the cervical ventral horn region of MND patients. Muscarinic cholinergic receptors, examined as specific [3H]quinuclidinylbenzilate ([3H]QNB) binding, was also highly concentrated in the ventral and dorsal gray matter of the control spinal cord, and was strongly reduced in the ventral horn region of MND patients, indicating a quite similar distribution pattern of ChAT activity. These biochemical changes of cholinergic transmission system may be paralleled to the morphological degeneration of the spinal lower motor neurons in MND patients. Activity of 2',3'-cyclic nucleotide-3'-phosphodiesterase (CNPase), a marker enzyme of central myelin structure, was evenly distributed throughout the whole spinal cord section, without regard to the gray and white matter, of both MND and control patients.
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PMID:Regional distribution of cholinergic neurons in human spinal cord transections in the patients with and without motor neuron disease. 628 85

Red blood cell and plasma cholinesterases were evaluated in control subjects and patients with the major forms of adult, sporadic motor neuron disease. For the purposes of this communication, the patients were considered as having amyotrophic lateral sclerosis (ALS) or its subtypes. Cholinesterase and acetylcholinesterase activities were evaluated and separated by dose response to their respective inhibitors. No kinetic differences were observed comparing red blood cell or plasma enzyme activities using either inhibitor. As found in previous studies, acetylcholinesterase accounted for more than 90% of acetylcholine hydrolysis in red blood cells. The plasma data were more complicated to evaluate, but at least 20% of total activity could be attributed to acetylcholinesterase. When red blood cell acetylcholinesterase activities of patients and controls were compared, no statistically significant difference was found. However, when plasma acetylcholinesterase activity was compared between the 2 groups, a statistically significant increase, almost twice the control value, was found in the ALS patients. These data may ultimately be important in the prognosis of this disease and, conceivably, could aid in understanding its pathogenesis.
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PMID:Plasma and red blood cell acetylcholinesterase in amyotrophic lateral sclerosis. 723 44

We reported a 63-year-old woman, suffered from myasthenia gravis with thymoma who later developed subacute motor neuronopathy after thymectomy. She noticed distally dominant muscle weakness and atrophy of bilateral upper extremities without sensory loss 4 month after thymomectomy. Her muscle weakness did not improve by intravenous administration of anti-cholinesterase (Tensilon test). Electrophysiological examinations showed no decremental response of examined muscles during repetitive nerve stimulation, nor motor nerve conduction block nor demyelination of affected peripheral nerves. Laboratory study demonstrated positive anti-acetylcholine receptor, anti-nuclear and SS-A antibodies. On immunohistochemistry, the patient's sera positively stained human and rat anterior horn cell cytoplasm as well as axoplasm of spinal white matter and root nerve axon, suggesting the presence of anti-axon antibody, possibly against neurofilament or tubulin components. The biopsied muscle specimen showed neurogenic muscle changes, but with no evidence of vasculitis nor cellular infiltration. Therapeutic trial of plasmapheresis was effective for her muscle weakness. Further recovery of weakness and muscle atrophy of hand muscles was obtained by combined therapy of intravenous and oral corticosteroid administration and plasmapheresis. These clinical, electrophysiological and histological findings suggested that antibodies against neuronal component might be responsible for her motor neuronopathy associated with myasthenia gravis. The findings of our case study may support the idea that some cases of motor neuron disease are caused by auto-immune mechanism.
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PMID:[Subacute motor neuronopathy associated with myasthenia gravis and thymoma]. 1054 13

A sensitive and specific enzyme linked immunosorbent assay (ELISA) utilizing human recombinant acetylcholinesterase has been employed for the detection of human antibodies to human acetylcholinesterase. The method can detect allogenic antibodies to the Yt(a) form of human erythrocyte AChE. Adaptation of this ELISA method allowed the IgG subclass typing of IgG anti-AChE antibodies, which could help to determine the possible role of these antibodies in the aetiology of any neurological conditions. Routine serological investigations established the AChE phenotype of each of the patients recruited, to determine whether anti-AChE antibodies were allogenic or autogenic in origin. These techniques were used to determine the incidence of autoantibodies to AChE in patients with neurological conditions, including the subtypes of motor neuron disease. The data presented are not consistent with earlier reports of a high incidence of autoantibodies to AChE in amyotrophic lateral sclerosis and progressive muscular atrophy.
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PMID:Autoantibodies to acetylcholinesterase revisited. 1086 90

Neuropathy target esterase (NTE) is a membrane protein found in human neurons and other cells, including lymphocytes. Binding of certain organophosphorus (OP) compounds to NTE is believed to cause OP-induced delayed neuropathy (OPIDN), a type of paralysis for which there is no effective treatment. Mutations in NTE have also been linked with serious neurological diseases, such as motor neuron disease. This paper describes development of the first nanostructured biosensor interface containing a catalytically active fragment of NTE known as NEST. The biosensor was fabricated using the layer-by-layer assembly approach, by immobilizing a layer of NEST on top of multilayers consisting of a polyelectrolyte (poly-L-lysine) and an enzyme (tyrosinase). The biosensor has a response time on the order of seconds and gives a concentration-dependent decrease in sensor output in response to a known NEST (and NTE) inhibitor. Potential applications of the biosensor include screening OP compounds for NTE inhibition and investigating the enzymology of wild-type and mutant forms of NTE. Although the development of a NEST biosensor was the primary purpose of this study, we found that the approach developed for NEST could also be extended to measure the activity of other esterases involved in neural processes, such as acetylcholinesterase (AChE) and butyrylcholinesterase (BChE). On the basis of measured sensitivities, phenyl valerate was the preferred substrate for NEST and BChE, whereas phenyl acetate was better for AChE.
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PMID:Nanostructured biosensor for measuring neuropathy target esterase activity. 1755 96


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