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)

A novel method to selectively lesion preganglionic sympathetic neurones has been combined with immunohistochemistry to study the expression of peptides in the rat superior cervical ganglion (SCG). Thus, systemic administration of monoclonal antibodies against acetylcholinesterase (AChE) caused a marked reduction in the number of enkephalin (ENK)-positive fibres and a total disappearance of fibres immunoreactive for calcitonin gene-related peptide (CGRP) and AChE in the SCG. A marked increase in the number of galanin/galanin message-associated peptide (GAL/GMAP)-immunoreactive cell bodies was also observed. The present results indicate that probably all CGRP and most ENK containing fibres in the rat SCG are of preganglionic origin and that peptides not normally expressed in SCG neurones, e.g. GAL and GMAP, can be upregulated after deafferentation.
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PMID:Effects of preganglionic sympathectomy on peptides in the rat superior cervical ganglion. 806 Dec 94

Previous work in our laboratory demonstrated that galantamine, a cholinesterase inhibitor and weak cholinergic agonist, facilitated classical trace eyeblink conditioning in healthy, young rabbits [Simon, B. B., Knuckley, B., & Powell, D. A. (2004). Galantamine facilitates acquisition of a trace-conditioned eyeblink response in healthy, young rabbits. Learning & Memory, 11(1), 116-122.]. The current study investigated the effects of galantamine (0.0 or 3.0mg/kg) in rabbits sustaining knife-cut lesions to the fimbria-fornix, a major projection pathway connecting the hippocampus to cortical and subcortical brain structures involved in the formation of long-term memories. Two experiments were conducted. Experiment one assessed the effects of knife-cut lesions to the fornix or sham surgeries on trace eyeblink (EB) conditioning. Results indicate that fornix lesions significantly retarded EB conditioning when trace parameters were employed. Experiment 2 assessed whether treatment with galantamine would reverse the deficits caused by fornix damage. Results indicate that 3.0mg/kg GAL reversed trace EB conditioning deficits in animals with fornix knife-cut lesions. These findings suggest that galantamine may provide benefit in the reversal of cognitive dysfunction following certain types of brain damage, especially damage involving hippocampal structures.
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PMID:Impairments in trace EB conditioning by knife-cut lesions to the fornix in rabbits: reversal by galantamine. 1761 52

The ability of galantamine hydrobromide (GAL HBr) treatment to antagonize O-ethyl-S-(2-diisopropylaminoethyl) methylphosphonothiolate (VX)-induced lethality, impairment of muscle tension, and electroencephalographic (EEG) changes was assessed in guinea pigs. Guinea pigs were challenged with 16.8 microg/kg VX (2LD50). One min after challenge, animals were administered 0.5 mg/kg atropine sulfate (ATR) and 25 mg/kg pyridine-2-aldoxime methochloride (2-PAM). In addition, guinea pigs were given 0, 1, 2, 4, 8 or 10 mg/kg GAL as a post-exposure treatment immediately prior to ATR and 2-PAM. Animals were either monitored for 24-h survival, scheduled for electroencephalography (EEG) recording, or euthanized 60 min later for measurement of indirectly-elicited muscle tension in the hemidiaphragm. Post-exposure GAL therapy produced a dose-dependent increase in survival from lethal VX challenge. Optimal clinical benefits were observed in the presence of 10 mg/kg GAL, which led to 100% survival of VX-challenged guinea pigs. Based on muscle physiology studies, GAL post-exposure treatment protected the guinea pig diaphragm, the major effector muscle of respiration, from fatigue, tetanic fade, and muscular paralysis. Protection against the paralyzing effects of VX was dose-dependent. In EEG studies, GAL did not alter seizure onset for all doses tested. At the highest dose tested (10 mg/kg), GAL decreased seizure duration when administered as a post-exposure treatment 1 min after VX. GAL also reduced the high correlation associated between seizure activity and lethality after 2LD50 VX challenge. GAL may have additional benefits both centrally and peripherally that are unrelated to its established mechanism as a reversible acetylcholinesterase inhibitor (AChEI).
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PMID:Galantamine is a novel post-exposure therapeutic against lethal VX challenge. 1964 7

Alzheimer's disease (AD) and vascular dementia (VaD) are the most common causes of dementia in the elderly. Although AD can be diagnosed with a considerable degree of accuracy, the distinction between isolated AD, VaD and mixed dementia (MD) [when both pathologies coexist in the same patient] remains a controversial issue and one of the most difficult diagnostic challenges. MD represents a very common pathology, especially in the elderly, as reported in neuropathological studies. Accurate diagnosis of MD is of crucial significance for epidemiological purposes and for preventive and therapeutic strategies. Until recently, pharmacological studies have generally focused on pure disease, either AD or VaD, and have provided few data on the best therapeutic approach to MD. There is only one original randomized clinical trial on (acetyl)cholinesterase inhibitor therapy (GAL-INT-6, galantamine) for MD; the other studies are post hoc analyses of AD trial subgroups (AD2000, donepezil) or of VaD trial subgroups (VantagE, rivastigmine). Cholinesterase inhibitors have reproducible beneficial effects on cognitive and functional outcomes in patients with MD. These benefits are of a similar magnitude to those previously reported for the treatment of AD. It is likely that the beneficial effects of memantine (an NMDA receptor antagonist) in AD may also apply to MD, but randomized controlled trials are still lacking. Treatment of cardiovascular risk factors, especially hypertension, may protect brain function and should be included in prevention strategies for MD.
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PMID:Management of mixed dementia. 2080 62