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)

Several neurotransmitter markers were investigated in the cerebrospinal fluid (CSF) from patients with Alzheimer's disease (AD) (n = 27), Parkinson's disease (PD) (n = 35) and ALS (n = 26) and from control subjects (n = 34) to compare the possible alterations in the biochemical profiles of these different neurodegenerative diseases. The main proportion of the patients represented an early phase of the illness at the time of the diagnosis. Correlations of the degree of dementia and the stage of the disease with CSF measures were evaluated. The CSF levels of somatostatin like-immunoreactivity (SLI) were significantly reduced in AD patients when compared with those of normals and ALS patients. The CSF concentrations of homovanillic acid (HVA) were significantly decreased for PD patients and the decrease focused on the non-demented patients. A trend of decreasing HVA values towards the most advanced stage of Parkinson's disease assessed by Webster's scale was also displayed. The content of 3-methoxy-4-hydroxyphenylglycol (MHPG) in the CSF was higher for ALS patients than for other groups. The lowest 5-hydroxy-indoleacetic acid (5HIAA) levels were observed in the PD group and the lowest acetylcholinesterase (AChE) activities were found in the PD patients with the most severe disease. Changes in CSF measures were too subtle to be beneficial for diagnostic purposes, but adequate for reflecting the different neurochemical profiles of these three degenerative neurological disorders.
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PMID:Neurochemical markers in the cerebrospinal fluid of patients with Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis and normal controls. 134 20

We analyzed binding sites for quinuclidinyl benzilate (QNB) and hemicholinium-3 (HC-3) by quantitative slice autoradiography and the activities of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) in spinal cord of 5-7 patients with amyotrophic lateral sclerosis (ALS). In the ventral horn, QNB binding sites were markedly reduced (38% of controls; P less than 0.001), whereas HC-3 binding sites were only moderately affected (76%, P less than 0.01). Losses in cholinergic marker enzymes were inconsistent. The loss of muscarinic binding sites in the ventral horn was the most reliable cholinergic disease marker in ALS.
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PMID:Cholinergic markers in ALS spinal cord. 162 47

The enzymatic activity of acetylcholinesterase (AchE) in the cerebrospinal fluid (CSF) is considered to be a marker of central cholinergic neuron integrity. Then, we evaluated CSF AchE activity in 90 cases of neurological diseases involving cholinergic system and their related disease, and 28 control cases without central organic lesions or abnormal findings in routine CSF study. AchE activity was evaluated according to Ellman's method using acetylthiocholine iodide as a substrate and tetraisopropyl-pyrophosphoramide, a specific inhibitor of butyrylocholinesterase. CSF AchE of Alzheimer type dementia (AD/SDAT, N = 12: 21.9 +/- 4.7 nmol/ml/min) showed no significant change from those of both control group (22.1 +/- 3.9) and vascular dementia (9: 21.7 +/- 6.7). In extrapyramidal diseases, reduction of the activity was observed in Huntington's chorea (HC, 4: 16.3 +/- 1.4) and progressive supranuclear palsy (PSP, 4: 17.6 +/- 1.7), whereas normal activity was shown in Parkinson's disease (PD, 19: 22.5 +/- 4.6), dentatorubropallidoluysian atrophy (DRPLA, 4: 22.6 +/- 4.2) and striatonigral degeneration (SND, 4: 20.4 +/- 4.3). In olivopontocerebellar atrophy (OPCA, N = 16), we disclosed reduced CSF AchE activity (15.8 +/- 2.4) which had significant correlations with the atrophy of the pontine base (r = 0.6017, p less than 0.02) and cerebellar vermis (r = 0.5450, p less than 0.05) in MRI. AchE activity in cerebellar cortical atrophy (CCA, 5: 20.6 +/- 2.2) remained within the control values. Normal activity was demonstrated in both amyotrophic lateral sclerosis (6: 24.3 +/- 7.3) and spinal muscular atrophy (4: 22.9 +/- 3.9).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[CSF acetylcholinesterase activity in central neurological diseases involving cholinergic systems]. 162 49

This article reports delayed dysneuria 143 cases, 54 cases in male and 89 cases in female, age 8-59 years old. They are treated by atropine. After the cholinesterase inhibited symptoms had vanished or had improved and after the other factors had been eliminated the delayed dysneurias occur after poisoning 5.42 days. They are the peripheral neuritis, the amyotrophic lateral sclerosis, the myasthenic crisis, the peptic neuritis, the encephalitis, the mixed aphasia and the symptoms like Guillain-Barre's syndrome. Their death rates are higher in two months to the types of the myasthenic crisis, the encephalitis and the amyotrophic lateral sclerosis and to the other types of disease and the cases. Poisoned two months later, their prognosis are better and the mechanism are not very clear now.
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PMID:[The report of organophosphorus pesticides cause delayed nervous system diseases (143 cases)]. 166 36

Serum acetylcholinesterase (AChE) and pseudocholinesterase (ChE) activity in infantile and juvenile spinal muscular atrophy (SMA) was determined. The total AChE activity was either normal or decreased in the childhood SMA (Type 1), the other SMA groups and disease controls (ALS, X-linked SMA). In the majority of SMA Type 1 cases (6/7 tested) an absence of the asymmetric A12 form was found. This was accompanied by changes in the other asymmetric and globular forms. The latter was, however, not specific for SMA Type 1 cases. The ChE activity was increased in the majority of SMA cases as well as disease controls. The asymmetric A12 ChE form was increased in all SMA Type 3 cases, the values of this form in SMA Type 1 was variable. A change in the ChE globular forms in SMA Type 1 and SMA Type 2 was a frequent finding. It is suggested that the absence of the asymmetric A12 AChE form in SMA Type 1 arises because of muscle cell immaturity and undeveloped muscle-nerve interactions. The reason of ChE changes is obscure.
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PMID:Serum cholinesterase activity in infantile and juvenile spinal muscular atrophy. 280 Oct 18

The purpose of this paper is to illustrate the advantages of the chemo-morphological approach in the study of pathological material. On one hand, the analysis of selected pathological cases (amputations, spinal transections) is able to provide invaluable information concerning the cells of origin of certain spinal transmitters in the human being. On the other hand, chemical neuropathology allows a more precise identification of the neuronal nets or types that are involved in a disease process. This advantage is underlined by studies performed in amyotrophic lateral sclerosis. In this condition, certain modifications, such as the reductions of acetylcholinesterase, choline acetyltransferase, cholinergic muscarinic, glycine or TRH receptors, are probably a consequence of motoneuron degeneration. In contradistinction, other findings, such as specific metabolic changes of motoneurons or early disappearance of SP-containing fibers in lamina IX, might be relevant for the pathogenesis of the disease.
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PMID:[Amyotrophic lateral sclerosis. Physiopathology and experimental models. Chemical neuroanatomy of the human spinal cord: applications to pathologic cases including amyotrophic lateral sclerosis]. 306 77

Human erythrocyte acetylcholinesterase (AChE) solubilized with Triton X-100 and obtained as a complex with micelles containing Triton and membrane phospholipids was incubated with immunoglobulins (Igs) from patients with amyotrophic lateral sclerosis (ALS) and from normal individuals. The temperature dependence of the AChE activity was determined. Biphasic (broken) Arrhenius plots were obtained with control Igs with the break point at 32.8 +/- 0.3 degrees C (SD, n = 18) indicating that the enzyme changes its conformation at this temperature. With ALS-Igs monophasic (linear) plots were observed in 14 cases and a biphasic in one case. ALS-Igs prevent the conformational change occurring at the break point temperature. The activation energy at physiological temperature increased by 60% from 2.4 to 3.8 kcal/mol (10.0-15.9 kJ/mol) which implies that ALS-Igs inhibit AChE. Thus, ALS-patients have autoantibodies that change the normal behaviour of erythrocyte AChE and which bind to the enzyme molecule or/and to phospholipids associated with the enzyme. At least part of the autoantibodies should be directed against the enzyme molecule, since a change in the Arrhenius plot was also observed in a control experiment with AChE which probably had micelles without any phospholipids. This enzyme was isolated by affinity chromatography and was washed with a buffer containing Triton X-100 before desorption from the affinity column, a treatment known to remove all phospholipids from erythrocyte AChE.
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PMID:Immunoglobulins from patients with amyotrophic lateral sclerosis affect human erythrocyte acetylcholinesterase. 322 Dec 39

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

Phrenic nerves of 11 patients with amyotrophic lateral sclerosis studied postmortem contained only 33% of the normal number of large myelinated fibers (9 controls; p less than 0.001). In the phrenic nerves of these patients, there were 18% fewer large myelinated fibers in the distal segment than in the proximal segment (p less than 0.025). The ratio of axonal circumference to myelin lamellae in large myelinated fibers in the distal segment was 34% greater than that in control fibers (p less than 0.002). The proportion of acute axonal degeneration was the same at all levels (48.0 +/- 13.7%). Sural nerves of 21 patients with amyotrophic lateral sclerosis had more acute axonal degeneration and 30% fewer myelinated fibers (p less than 0.05) than controls; evidence of degeneration also extended to unmyelinated fibers. The amount of axonal transport of acetylcholinesterase in 9 sural nerves determined in vitro was reduced by 24% (p less than 0.05) and the apparent transport rate was reduced by 44% (p less than 0.01) compared with 4 controls. These findings show that in amyotrophic lateral sclerosis a small degree of dying-back change and of distal axonal atrophy is superimposed on the degeneration of motor neuron cell bodies, and that the disease effects spread beyond the motor neurons.
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PMID:Morphometric and biochemical studies of peripheral nerves in amyotrophic lateral sclerosis. 619 54

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


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