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 intralaminar distributions of transmitter and nontransmitter enzyme activities and amino acid levels were determined in the midtemporal cortices from normal individuals and established cases of Alzheimer's disease. In the normal, choline acetyltransferase (CAT) and acetylcholinesterase (AChE) activities were relatively high in the outer cortical layers, particularly, for CAT, in the two granular layers (II and IV). Both activities were reduced in Alzheimer's disease at all, although generally most extensively in the outer and middle layers of the grey matter whereas activities were near normal in the white matter. Further, the enzyme distribution patterns of these cholinergic activities were also disrupted in Alzheimer's disease and the activity of CAT throughout the cortex was generally reduced to that found in the white matter. No such differences in distribution were found for two other enzymes, pseudocholinesterase and lactate dehydrogenase. Assessment of the gamma-aminobutyric acid (GABA) system in the normal revealed a much more extensive intralaminar variation in the enzyme, glutamate decarboxylase, compared with the level of GABA itself. In contrast with the cholinergic enzymes, neither the levels nor intralaminar patterns of GABA were altered in Alzheimer's disease. From an analysis of free amino acids at the different cortical levels, the cortical pattern of glutamic acid in the normal was different from that for GABA, aspartic acid, or nontransmitter amino acids such as alanine. Neither of the putative amino acids, glutamate or aspartate, was altered in Alzheimer's disease. These findings demonstrate the relatively selective nature of microchemical changes occurring in the cortex in Alzheimer's disease and suggest that a functional abnormality in cholinergic input to the outer neocortical layers (I-IV) with predominantly receptive and associative functions may be an important feature of the disease.
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PMID:Intralaminar neurochemical distributions in human midtemporal cortex: comparison between Alzheimer's disease and the normal. 614 24

The pesticide trichlorfon (125 mg/kg on days 42-44 in gestation) gives hypoplasia of the brain of the offspring without any significant reduction in their body weights. The hypoplasia may be caused by trichlorfon itself or by its metabolite dichlorvos. This period of development coincides with the growth spurt period of guinea pig brain. The largest changes occurred in the cerebellum. Electron microscopic examination of the cerebellar cortex showed increased apoptotic death of cells in the granule cell layer after trichlorfon treatment. A reduction in thickness of the external germinal layer of the cerebellar cortex and an elevated amount of pyknotic and karyorrhexic cells in the granule cell layer was found. There was a significant reduction in choline esterase, choline acetyltransferase and glutamate decarboxylase activities in the cerebellum. Methylazoxymethanol (15 mg/kg body weight, day 43) was examined for comparison and caused similar hypoplasia of the guinea pig cerebellum, but did also induce a reduction in body weight. Trichloroethanol, the main metabolite of trichlorfon, did not give brain hypoplasia.
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PMID:The effect of trichlorfon and methylazoxymethanol on the development of guinea pig cerebellum. 1715 Feb 36