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)

Chronic brain inflammation is the common final pathway in the majority of neurodegenerative diseases and central to this phenomenon is the immunological activation of brain mononuclear phagocyte cells, called microglia. This inflammatory mechanism is a central component of HIV-associated dementia (HAD). In the healthy state, there are endogenous signals from neurons and astrocytes, which limit excessive central nervous system (CNS) inflammation. However, the signals controlling this process have not been fully elucidated. Studies on the peripheral nervous system suggest that a cholinergic anti-inflammatory pathway regulates systemic inflammatory response by way of acetylcholine acting at the alpha7 nicotinic acetylcholine receptor (alpha7nAChR) found on blood-borne macrophages. Recent data from our laboratory indicates that cultured microglial cells also express this same receptor and that microglial anti-inflammatory properties are mediated through it and the p44/42 mitogen-activated protein kinase (MAPK) system. Here we report for the first time the creation of an in vitro model of HAD composed of cultured microglial cells synergistically activated by the addition of IFN-gamma and the HIV-1 coat glycoprotein, gp120. Furthermore, this activation, as measured by TNF-alpha and nitric oxide (NO) release, is synergistically attenuated through the alpha7 nAChR and p44/42 MAPK system by pretreatment with nicotine, and the cholinesterase inhibitor, galantamine. Our findings suggest a novel therapeutic combination to treat or prevent the onset of HAD through this modulation of the microglia inflammatory mechanism.
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PMID:Galantamine and nicotine have a synergistic effect on inhibition of microglial activation induced by HIV-1 gp120. 1534 4

Highly reactive horses may pose risks to humans involved in equestrian activities. Among the factors that may affect horses' reactivity to external stimuli are pesticides used for fly control in equine facilities. The organophosphorus (OP) insecticide tetrachlorvinphos (TCVP) is used as a feed-through larvicide to prevent completion of the fly larval life cycle in horse manure. TCVP exerts its effect by inhibiting the enzyme cholinesterase (ChE) leading to the accumulation of the neurotransmitter acetylcholine (AChE) in synapses of the central and peripheral nervous systems. The aim of the present study was to investigate alterations of whole-blood ChE levels associated with feeding a commercially available product (Equitrol, Farnam Companies, Inc.) to horses for fly control. A second aim was to report neurological, physiological and behavioural findings in addition to profiles of selected immune markers (IFN-gamma, IL-12p40 and COX-2) and serum thyroid hormones during and after a 30-day treatment period of TCVP feeding. The results indicated significant decreases in whole-blood ChE activity and concomitant behavioural alterations, manifested as increased reactivity and decreased controllability in treated horses. No changes were detected in physiological or neurological parameters, immune markers or thyroid hormones in treated (n=6) or control (n=4) horses during the course of the study.
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PMID:Effects of oral tetrachlorvinphos fly control (Equitrol) administration in horses: physiological and behavioural findings. 1752 60