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)

Eight liver biopsy specimens from five patients with PAS-negative intracisternal hyalin were investigated by immunofluorescence for: (1) immunoglobulins (Ig) G, A, M, D, E; (2) light chains (kappa and lambda); (3) complement components C1q, C4, C3c, C5, C9; (4) C1-inactivator; (5) C3-activator; (6) alpha 1-antitrypsin; (7) alpha 1-antichymotrypsin; (8) plasminogen; (9) fibrinogen; (10) fibrinogen breakdown products D and E; (11) fibronectin; (12) prealbumin; (13) albumin; (14) betalipoprotein; (15) apolipoprotein; (16) alpha 1- and alpha 2-glycoprotein; (17) cholinesterase; (18) ceruloplasmin; (19) haemopexin; (20) myoglobin; (21) placenta lactogen; (22) transferrin; (23) actin; (24) myosin; (25) cathepsin D; and (26) hepatitis B surface and core antigens (HBsAg and HBcAg). The globules reacted significantly with antisera against C3c (three patients), C4 (three patients), C3-activator (one patient) and fibrinogen (two patients). The cause of the protein accumulation is not clear. Serial studies indicate the possibility of a disturbance of protein secretion and an as yet unidentified immune complex disorder.
 ...
PMID:Immunohistological investigations of PAS-negative globular intracisternal hyalin in human liver biopsy specimens. 285 88

To assess the sensitivity, specificity and clinical value of prealbumin as liver test, prealbumin plasma levels were measured in 100 patients with liver disease and in 65 patients without clinical evidence of liver impairment. The sensitivity of prealbuminemia was higher than that of albumin, pseudocholinesterase, apolipoprotein and prothrombin activity. Its specificity was higher than that of pseudocholinesterase and comparable with the specificity of other liver tests. Prealbumin plasma levels were progressively decreasing in patients with liver cirrhosis graded as Child's A, B and C, respectively. In these patients prealbuminemia was correlated with galactose elimination capacity, assumed to be an index of maximal liver functional capacity.
 ...
PMID:Value of prealbumin plasma levels as liver test. 362 40

Alzheimer's disease is a progressive degenerative disease with cognitive and behavioral manifestations. The pathophysiology of Alzheimer's disease is increasingly well understood, leading to approved and experimental therapies. Mutations on chromosomes 1, 14, and 21 can cause the disease and are sometimes present in patients with early onset Alzheimer's disease. Older patients--comprising the majority of Alzheimer's disease victims--have a variety of risk factors including age, gender, history of head trauma, low education level, and apolipoprotein genotype. The pathogenetic process leads to regional cell loss and biochemical deficits. The mutations and risk factors lead to increased amyloid production or accumulation and nerve cell death. Neurons atrophy in the cerebral cortex and in source nuclei of important neurotransmitters. The deficiency of acetylcholine can be partially remedied by cholinesterase inhibitors that produce modest cognitive and behavioral improvement. Anti-amyloid agents, antioxidants, anti-inflammatory drugs, estrogens, and calcium channel blockers may all slow the progression of Alzheimer's disease by interfering with specific steps within the disease cascade. Neuropsychiatric symptoms are also common in Alzheimer's disease and may be ameliorated by conventional psychotropic agents. Clinicians can currently offer substantial help to Alzheimer's disease patients, and the future promises more effective pharmacotherapy.
 ...
PMID:Alzheimer's disease: cognitive and behavioral pharmacotherapy. 933 9

We investigated the effects of a single administration of tetrahydroaminoacridine (25 and 50 mg, orally), a cholinesterase inhibitor, on memory function in Alzheimer's disease patients. The recall of memory items from the end of the word list (recency effect) was improved in a subgroup of Alzheimer's disease patients (responders 10 out of 28) by tetrahydroaminoacridine 50 mg. However, tetrahydroaminoacridine 50 mg had no effect on the recall of those words from the beginning or middle of the list. Tetrahydroaminoacridine did not markedly improve non-verbal delayed matching to sample or paired associates learning in any of the Alzheimer's disease patients. The "responders" performed better than the "non-responders" in tests measuring memory and frontal functions. The responders had less severe hippocampal atrophy and less prefrontal blood flow defect, and had a lower frequency of the apolipoprotein E4 allele than the "non-responders". These results suggest that acute tetrahydroaminoacridine treatment may stimulate the recency effect, and that a severe dysfunction of hippocampus and prefrontal regions blocks this effect of tetrahydroaminoacridine on short-term memory performance.
 ...
PMID:Tetrahydroaminoacridine improves the recency effect in Alzheimer's disease. 946 Jul 55

The polymorphic K variant of the butyrylcholinesterase ( BCHE-K ) gene recently has been demonstrated to have an elevated frequency in Alzheimer's disease (AD) patients carrying the epsilon4 allele of the apolipoprotein (APO E) gene when compared with a control population. We therefore genotyped a large series of pathologically confirmed AD patients and controls to confirm this association. We found no change in the frequency of this genetic variant, either in the AD group as a whole or in early- or late-onset patients when compared with age-matched controls. Stratification of these groups with reference to the APO E epsilon4 allele also showed no difference between AD and control groups. To determine if a biological effect were present, we also looked at senile plaque and neurofibrillary tangle densities in the frontal, temporal, parietal and occipital cortices in AD patients either carrying or not carrying a copy of the K variant. We found no difference in plaque or tangle load between these two groups in either the total, late-onset or early-onset AD subjects. Stratification of the total AD group in terms of APO E epsilon4 allele possession, and further comparison of plaque and tangle load between carriers and non-carriers of BCHE-K still failed to disclose a relationship between BCHE-K and AD. We conclude that in the population studied here there is no association between BCHE-K and AD, or that if such a relationship exists it is precluded by another, as yet unknown factor.
 ...
PMID:No association between the K variant of the butyrylcholinesterase gene and pathologically confirmed Alzheimer's disease. 953

A recent study has linked the butyrylcholinesterase (BChE) K-variant and the apolipoprotein epsilon4 isoform to late-onset Alzheimer's disease. These findings have been controversial and have led us to examine the differences between wild-type and K-variant BChE in enzyme activity, protein stability, and quaternary structure. J-variant BChE (E497V/A539T) was also studied because it is associated with the K-variant mutation. The K-variant mutation (A539T) is located in the C-terminal tetramerization domain. Wild-type, K-variant, and J-variant BChE were expressed in Chinese hamster ovary cells and purified. The purified enzymes had similar binding affinity (Km) values and catalytic rates for butyrylthiocholine and benzoylcholine. In pulse-chase studies the K-variant, J-variant, and wildtype BChE were degraded rapidly within the cell, with a half-time of approximately 1.5 h. Less than 5% of the intracellular BChE was exported. The C-terminal peptide containing the K-variant mutation interacted with itself as strongly as did the wild-type peptide in the yeast two-hybrid system. Both K-variant and wild-type BChE assembled into tetramers in the presence of poly-L-proline or the proline-rich attachment domain of the collagen tail. The native K-variant BChE in serum showed the same proportion of tetramers as the native serum wild-type BChE. We conclude that the K-variant BChE is similar to wild-type BChE in enzyme activity, protein turnover, and tetramer formation.
 ...
PMID:The butyrylcholinesterase K-variant shows similar cellular protein turnover and quaternary interaction to the wild-type enzyme. 1064 40

Cholinesterase inhibitors improve cognition and behaviour in some patients with Alzheimer's disease (AD). Studies that have focused on methods to predict response to anticholinesterase therapy and markers for response are reviewed. Among the possible predictors of improvement in cognitive outcomes are apolipoprotein genotype, pretreatment postural blood pressure drop, quantitative electroencephalography (qEEG) and disease progression rate. Of these, qEEG profile after a single dose of an acetylcholinesterase inhibitor was consistently found to be a good predictor of cognitive response. Studies have assessed baseline behavioural profiles and baseline single-photon emission computed tomographic profiles as possible predictors of improvement of behavioural symptoms of AD, but these require further study. Possible markers of response during drug treatment include red blood cell cholinesterase inhibition, cerebrospinal fluid monoamine measurement, pupillary response and platelet amyloid precursor protein analyses. Although they, too, require further study, the analysis of platelet amyloid precursor protein may have value as a correlate of the putative disease-modifying effects of long-term treatment. Studying correlates of response may help to elucidate the mechanism of action of acetylcholinesterase inhibitors.
 ...
PMID:Correlates of response to acetylcholinesterase inhibitor therapy in Alzheimer's disease. 1258 47

The inheritance of the apolipoprotein E4 (APOE4) allele has been shown to increase the plasma cholesterol level, but little information is as concerns the association of the APOE genotype and hyperlipidaemia and the activities of two serum enzymes, acetylcholinesterase (AChE) and butyrylcholinesterase (BChE). Blood samples from 55 type IIb hyperlipidaemic, non-demented patients and 55 age- and sex-matched controls were therefore examined in this pilot study. A significantly increased BChE activity was found in the serum of type IIb hyperlipidaemic patients, but the AChE activity did not differ significantly as compared with that in the control group. The APOE4 allele was significantly overrepresented among the hyperlipidaemic probands, but neither serum cholinesterase activity was affected by the dosage of the APOE4 gene. Our results point to a possible association between an abnormal lipid metabolism and the BChE activity and might have implications as regards the pathomechanism of both Alzheimer's and vascular dementias and the cholinesterase inhibitor therapy of dementing disorders.
 ...
PMID:Increased serum butyrylcholinesterase activity in type IIb hyperlipidaemic patients. 1521 7

Serum apolipoprotein B (apo B) levels were found to be significantly (p < 0.001) higher in the 27 patients with combined hyperlipidemia (144 m./dl +/- 27.6) than in the 17 normal weight normolipidemic control subjects (92 mg/dl +/- 20.6; X +/- SD). When compared to apolipoprotein A1 (apo A1) levels obtained in controls (168.5 mg/dl +/- 28.4), hyperlipidemic subjects displayed a moderate yet significant (p < 0.02) decrease of this apolipoprotein (140 mg/dl +/- 24.2). Serum apo B levels were significantly (p < 0.001) correlated with serum cholesterol concentrations and also, to a lesser degree (p < 0.01), with serum cholinesterase activity. A highly significant correlation (p < 0.001) between apo A1 and HDL cholesterol levels was also noted. The decrease ofHDL cholesterol occurring in hyperlipidemic men (-30%) was however more accentuated than the decrease of apo A1 (-18%) suggesting an enhanced transfer of cholesterol esters from HDL to VLDL and LDL. It is considered that the determination of apolipoproteins may be useful not only for the detection of risk factors for atherosclerosis, but also for a better insight concerning the mechanisms involved in the development of an atherogenic dyslipidemia.
 ...
PMID:Apolipoproteins A1 and B levels and serum cholinesterase activity in hyperlipidemic subjects. 1552 47

Extracellular amyloid plaques, intracellular neurofibrillary tangles, and loss of basal forebrain cholinergic neurons in the brains of Alzheimer's disease (AD) patients may be the end result of abnormalities in lipid metabolism and peroxidation that may be caused, or exacerbated, by beta-amyloid peptide (Abeta). Apolipoprotein E (apoE) is a major apolipoprotein in the brain, mediating the transport and clearance of lipids and Abeta. ApoE-dependent dendritic and synaptic regeneration may be less efficient with apoE4, and this may result in, or unmask, age-related neurodegenerative changes. The increased risk of AD associated with apoE4 may be modulated by diet, vascular risk factors, and genetic polymorphisms that affect the function of other transporter proteins and enzymes involved in brain lipid homeostasis. Diet and apoE lipoproteins influence membrane lipid raft composition and the properties of enzymes, transporter proteins, and receptors mediating Abeta production and degradation, tau phosphorylation, glutamate and glucose uptake, and neuronal signal transduction. The level and isoform of apoE may influence whether Abeta is likely to be metabolized or deposited. This review examines the current evidence for diet, lipid homeostasis, and apoE in the pathogenesis of AD. Effects on the cholinergic system and response to cholinesterase inhibitors by APOE allele carrier status are discussed briefly.
 ...
PMID:Lipid homeostasis and apolipoprotein E in the development and progression of Alzheimer's disease. 1571 86


1 2 Next >>