Drugs that inhibit cholinesterases. The neurotransmitter ACETYLCHOLINE is rapidly hydrolyzed, and thereby inactivated, by cholinesterases. When cholinesterases are inhibited, the action of endogenously released acetylcholine at cholinergic synapses is potentiated. Cholinesterase inhibitors are widely used clinically for their potentiation of cholinergic inputs to the gastrointestinal tract and urinary bladder, the eye, and skeletal muscles; they are also used for their effects on the heart and the central nervous system.
Phenyl esters of carbamic acid or of N-substituted carbamic acids. Structures are similar to PHENYLUREA COMPOUNDS with a carbamate in place of the urea.
Aryl CYCLOPENTANES that are a reduced (protonated) form of INDENES.
A benzazepine derived from norbelladine. It is found in GALANTHUS and other AMARYLLIDACEAE. It is a cholinesterase inhibitor that has been used to reverse the muscular effects of GALLAMINE TRIETHIODIDE and TUBOCURARINE and has been studied as a treatment for ALZHEIMER DISEASE and other central nervous system disorders.
A cholinesterase inhibitor that crosses the blood-brain barrier. Tacrine has been used to counter the effects of muscle relaxants, as a respiratory stimulant, and in the treatment of Alzheimer's disease and other central nervous system disorders.
An aspect of cholinesterase (EC
A cholinesterase inhibitor that is rapidly absorbed through membranes. It can be applied topically to the conjunctiva. It also can cross the blood-brain barrier and is used when central nervous system effects are desired, as in the treatment of severe anticholinergic toxicity.
An enzyme that catalyzes the hydrolysis of ACETYLCHOLINE to CHOLINE and acetate. In the CNS, this enzyme plays a role in the function of peripheral neuromuscular junctions. EC
AMANTADINE derivative that has some dopaminergic effects. It has been proposed as an antiparkinson agent.
A cholinesterase inhibitor used in the treatment of myasthenia gravis and to reverse the effects of muscle relaxants such as gallamine and tubocurarine. Neostigmine, unlike PHYSOSTIGMINE, does not cross the blood-brain barrier.
Drugs used to specifically facilitate learning or memory, particularly to prevent the cognitive deficits associated with dementias. These drugs act by a variety of mechanisms. While no potent nootropic drugs have yet been accepted for general use, several are being actively investigated.
A carbamate insecticide with anticholinesterase activity.
A cholinesterase inhibitor that is used as an organothiophosphorus insecticide.
A cholinesterase inhibitor with a slightly longer duration of action than NEOSTIGMINE. It is used in the treatment of myasthenia gravis and to reverse the actions of muscle relaxants.
A family of hexahydropyridines.
A rapid-onset, short-acting cholinesterase inhibitor used in cardiac arrhythmias and in the diagnosis of myasthenia gravis. It has also been used as an antidote to curare principles.
An organochlorophosphate cholinesterase inhibitor that is used as an insecticide for the control of flies and roaches. It is also used in anthelmintic compositions for animals. (From Merck, 11th ed)
A degenerative disease of the BRAIN characterized by the insidious onset of DEMENTIA. Impairment of MEMORY, judgment, attention span, and problem solving skills are followed by severe APRAXIAS and a global loss of cognitive abilities. The condition primarily occurs after age 60, and is marked pathologically by severe cortical atrophy and the triad of SENILE PLAQUES; NEUROFIBRILLARY TANGLES; and NEUROPIL THREADS. (From Adams et al., Principles of Neurology, 6th ed, pp1049-57)
A highly toxic cholinesterase inhibitor that is used as an acaricide and as an insecticide.
Compounds containing carbon-phosphorus bonds in which the phosphorus component is also bonded to one or more sulfur atoms. Many of these compounds function as CHOLINERGIC AGENTS and as INSECTICIDES.
An organothiophosphate cholinesterase inhibitor that is used as an insecticide and as an acaricide.
An organophosphorus ester compound that produces potent and irreversible inhibition of cholinesterase. It is toxic to the nervous system and is a chemical warfare agent.
An organothiophosphate insecticide.
Pesticides designed to control insects that are harmful to man. The insects may be directly harmful, as those acting as disease vectors, or indirectly harmful, as destroyers of crops, food products, or textile fabrics.
An organophosphorus compound that inhibits cholinesterase. It causes seizures and has been used as a chemical warfare agent.
A potent, long-acting cholinesterase inhibitor used as a miotic in the treatment of glaucoma.
An organophosphate cholinesterase inhibitor that is used as a pesticide.
A neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.
Carbamate derivative used as an insecticide, acaricide, and nematocide.
Derivatives of carbamic acid, H2NC(=O)OH. Included under this heading are N-substituted and O-substituted carbamic acids. In general carbamate esters are referred to as urethanes, and polymers that include repeating units of carbamate are referred to as POLYURETHANES. Note however that polyurethanes are derived from the polymerization of ISOCYANATES and the singular term URETHANE refers to the ethyl ester of carbamic acid.
Drugs that bind to but do not activate MUSCARINIC RECEPTORS, thereby blocking the actions of endogenous ACETYLCHOLINE or exogenous agonists. Muscarinic antagonists have widespread effects including actions on the iris and ciliary muscle of the eye, the heart and blood vessels, secretions of the respiratory tract, GI system, and salivary glands, GI motility, urinary bladder tone, and the central nervous system.
An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness.
Chemicals that are used to cause the disturbance, disease, or death of humans during WARFARE.
Drugs that mimic the effects of parasympathetic nervous system activity. Included here are drugs that directly stimulate muscarinic receptors and drugs that potentiate cholinergic activity, usually by slowing the breakdown of acetylcholine (CHOLINESTERASE INHIBITORS). Drugs that stimulate both sympathetic and parasympathetic postganglionic neurons (GANGLIONIC STIMULANTS) are not included here.
Drugs used to reverse the inactivation of cholinesterase caused by organophosphates or sulfonates. They are an important component of therapy in agricultural, industrial, and military poisonings by organophosphates and sulfonates.
Organic compounds that contain phosphorus as an integral part of the molecule. Included under this heading is broad array of synthetic compounds that are used as PESTICIDES and DRUGS.
Method of psychotherapeutic treatment based on assumption of patients' personal responsibility for their own behavior. The therapist actively guides patients to accurate self-perception for fulfillment of needs of self-worth and respect for others. (From APA, Thesaurus of Psychological Index Terms, 8th ed.)
A mercaptocholine used as a reagent for the determination of CHOLINESTERASES. It also serves as a highly selective nerve stain.
An aspect of cholinesterases.
Neurologic disorders caused by exposure to toxic substances through ingestion, injection, cutaneous application, or other method. This includes conditions caused by biologic, chemical, and pharmaceutical agents.
A highly fluorescent anti-infective dye used clinically as a topical antiseptic and experimentally as a mutagen, due to its interaction with DNA. It is also used as an intracellular pH indicator.
An alkaloid, originally from Atropa belladonna, but found in other plants, mainly SOLANACEAE. Hyoscyamine is the 3(S)-endo isomer of atropine.
A basic constituent of lecithin that is found in many plants and animal organs. It is important as a precursor of acetylcholine, as a methyl donor in various metabolic processes, and in lipid metabolism.
A local anesthetic of the amide type now generally used for surface anesthesia. It is one of the most potent and toxic of the long-acting local anesthetics and its parenteral use is restricted to spinal anesthesia. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1006)
Any drugs that are used for their effects on dopamine receptors, on the life cycle of dopamine, or on the survival of dopaminergic neurons.
Drugs that bind to and activate muscarinic cholinergic receptors (RECEPTORS, MUSCARINIC). Muscarinic agonists are most commonly used when it is desirable to increase smooth muscle tone, especially in the GI tract, urinary bladder and the eye. They may also be used to reduce heart rate.
One of the two major classes of cholinergic receptors. Muscarinic receptors were originally defined by their preference for MUSCARINE over NICOTINE. There are several subtypes (usually M1, M2, M3....) that are characterized by their cellular actions, pharmacology, and molecular biology.
N,N',N'',N'''-Tetraisopropylpyrophosphamide. A specific inhibitor of pseudocholinesterases. It is commonly used experimentally to determine whether pseudo- or acetylcholinesterases are involved in an enzymatic process.
The relationship between the dose of an administered drug and the response of the organism to the drug.
A neurodegenerative disease characterized by dementia, mild parkinsonism, and fluctuations in attention and alertness. The neuropsychiatric manifestations tend to precede the onset of bradykinesia, MUSCLE RIGIDITY, and other extrapyramidal signs. DELUSIONS and visual HALLUCINATIONS are relatively frequent in this condition. Histologic examination reveals LEWY BODIES in the CEREBRAL CORTEX and BRAIN STEM. SENILE PLAQUES and other pathologic features characteristic of ALZHEIMER DISEASE may also be present. (From Neurology 1997;48:376-380; Neurology 1996;47:1113-1124)
Drugs that bind to but do not activate CHOLINERGIC RECEPTORS, thereby blocking the actions of ACETYLCHOLINE or cholinergic agonists.
An organophosphorus insecticide that inhibits ACETYLCHOLINESTERASE.
Standardized clinical interview used to assess current psychopathology by scaling patient responses to the questions.
Cardiac arrhythmias that are characterized by excessively slow HEART RATE, usually below 50 beats per minute in human adults. They can be classified broadly into SINOATRIAL NODE dysfunction and ATRIOVENTRICULAR BLOCK.
Any drug used for its actions on cholinergic systems. Included here are agonists and antagonists, drugs that affect the life cycle of ACETYLCHOLINE, and drugs that affect the survival of cholinergic neurons. The term cholinergic agents is sometimes still used in the narrower sense of MUSCARINIC AGONISTS, although most modern texts discourage that usage.
Various salts of a quaternary ammonium oxime that reconstitute inactivated acetylcholinesterase, especially at the neuromuscular junction, and may cause neuromuscular blockade. They are used as antidotes to organophosphorus poisoning as chlorides, iodides, methanesulfonates (mesylates), or other salts.
A quaternary skeletal muscle relaxant usually used in the form of its bromide, chloride, or iodide. It is a depolarizing relaxant, acting in about 30 seconds and with a duration of effect averaging three to five minutes. Succinylcholine is used in surgical, anesthetic, and other procedures in which a brief period of muscle relaxation is called for.
The craniosacral division of the autonomic nervous system. The cell bodies of the parasympathetic preganglionic fibers are in brain stem nuclei and in the sacral spinal cord. They synapse in cranial autonomic ganglia or in terminal ganglia near target organs. The parasympathetic nervous system generally acts to conserve resources and restore homeostasis, often with effects reciprocal to the sympathetic nervous system.
The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.
An organothiophosphate cholinesterase inhibitor that is used as an insecticide.
A carbamate insecticide and parasiticide. It is a potent anticholinesterase agent belonging to the carbamate group of reversible cholinesterase inhibitors. It has a particularly low toxicity from dermal absorption and is used for control of head lice in some countries.
Cell surface proteins that bind acetylcholine with high affinity and trigger intracellular changes influencing the behavior of cells. Cholinergic receptors are divided into two major classes, muscarinic and nicotinic, based originally on their affinity for nicotine and muscarine. Each group is further subdivided based on pharmacology, location, mode of action, and/or molecular biology.
Tests designed to assess neurological function associated with certain behaviors. They are used in diagnosing brain dysfunction or damage and central nervous system disorders or injury.
An imprecise term referring to dementia associated with CEREBROVASCULAR DISORDERS, including CEREBRAL INFARCTION (single or multiple), and conditions associated with chronic BRAIN ISCHEMIA. Diffuse, cortical, and subcortical subtypes have been described. (From Gerontol Geriatr 1998 Feb;31(1):36-44)
A sulfur-containing analog of butyrylcholine which is hydrolyzed by butyrylcholinesterase to butyrate and thiocholine. It is used as a reagent in the determination of butyrylcholinesterase activity.
Disturbances in mental processes related to learning, thinking, reasoning, and judgment.
An agent used as a substrate in assays for cholinesterases, especially to discriminate among enzyme types.
Organic nitrogenous bases. Many alkaloids of medical importance occur in the animal and vegetable kingdoms, and some have been synthesized. (Grant & Hackh's Chemical Dictionary, 5th ed)
A di-isopropyl-fluorophosphate which is an irreversible cholinesterase inhibitor used to investigate the NERVOUS SYSTEM.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
A method of studying a drug or procedure in which both the subjects and investigators are kept unaware of who is actually getting which specific treatment.
Drugs that bind to but do not activate excitatory amino acid receptors, thereby blocking the actions of agonists.
The benzoic acid ester of choline.
Amide derivatives of phosphoric acid such as compounds that include the phosphoric triamide (P(=O)(N)(N)(N)) structure.
Intellectual or mental process whereby an organism obtains knowledge.
One of the two major classes of cholinergic receptors. Nicotinic receptors were originally distinguished by their preference for NICOTINE over MUSCARINE. They are generally divided into muscle-type and neuronal-type (previously ganglionic) based on pharmacology, and subunit composition of the receptors.
Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids.
Drugs that bind to nicotinic cholinergic receptors (RECEPTORS, NICOTINIC) and block the actions of acetylcholine or cholinergic agonists. Nicotinic antagonists block synaptic transmission at autonomic ganglia, the skeletal neuromuscular junction, and at central nervous system nicotinic synapses.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
The action of a drug that may affect the activity, metabolism, or toxicity of another drug.
Chemicals used to destroy pests of any sort. The concept includes fungicides (FUNGICIDES, INDUSTRIAL); INSECTICIDES; RODENTICIDES; etc.
Agents that control agitated psychotic behavior, alleviate acute psychotic states, reduce psychotic symptoms, and exert a quieting effect. They are used in SCHIZOPHRENIA; senile dementia; transient psychosis following surgery; or MYOCARDIAL INFARCTION; etc. These drugs are often referred to as neuroleptics alluding to the tendency to produce neurological side effects, but not all antipsychotics are likely to produce such effects. Many of these drugs may also be effective against nausea, emesis, and pruritus.
A carbamate insecticide.
Nicotine is highly toxic alkaloid. It is the prototypical agonist at nicotinic cholinergic receptors where it dramatically stimulates neurons and ultimately blocks synaptic transmission. Nicotine is also important medically because of its presence in tobacco smoke.
The communication from a NEURON to a target (neuron, muscle, or secretory cell) across a SYNAPSE. In chemical synaptic transmission, the presynaptic neuron releases a NEUROTRANSMITTER that diffuses across the synaptic cleft and binds to specific synaptic receptors, activating them. The activated receptors modulate specific ion channels and/or second-messenger systems in the postsynaptic cell. In electrical synaptic transmission, electrical signals are communicated as an ionic current flow across ELECTRICAL SYNAPSES.
A plant family of the order Euphorbiales, subclass Rosidae, class Magnoliopsida. Leaves are alternate, simple, and leathery. Fruits are one- or two-seeded capsules or drupes (stony-pitted fleshy fruits).

Metrifonate increases neuronal excitability in CA1 pyramidal neurons from both young and aging rabbit hippocampus. (1/1796)

The effects of metrifonate, a second generation cholinesterase inhibitor, were examined on CA1 pyramidal neurons from hippocampal slices of young and aging rabbits using current-clamp, intracellular recording techniques. Bath perfusion of metrifonate (10-200 microM) dose-dependently decreased both postburst afterhyperpolarization (AHP) and spike frequency adaptation (accommodation) in neurons from young and aging rabbits (AHP: p < 0.002, young; p < 0.050, aging; accommodation: p < 0.024, young; p < 0.001, aging). These reductions were mediated by muscarinic cholinergic transmission, because they were blocked by addition of atropine (1 microM) to the perfusate. The effects of chronic metrifonate treatment (12 mg/kg for 3 weeks) on CA1 neurons of aging rabbits were also examined ex vivo. Neurons from aging rabbits chronically treated with metrifonate had significantly reduced spike frequency accommodation, compared with vehicle-treated rabbits. Chronic metrifonate treatment did not result in a desensitization to metrifonate ex vivo, because bath perfusion of metrifonate (50 microM) significantly decreased the AHP and accommodation in neurons from both chronically metrifonate- and vehicle-treated aging rabbits. We propose that the facilitating effect of chronic metrifonate treatment on acquisition of hippocampus-dependent tasks such as trace eyeblink conditioning by aging subjects may be caused by this increased excitability of CA1 pyramidal neurons.  (+info)

Comparison of two in vitro activation systems for protoxicant organophosphorous esterase inhibitors. (2/1796)

In order to perform in vitro testing of esterase inhibition caused by organophosphorous (OP) protoxicants, simple, reliable methods are needed to convert protoxicants to their esterase-inhibiting forms. Incubation of parathion or chlorpyrifos with 0.05% bromine solution or uninduced rat liver microsomes (RLM) resulted in production of the corresponding oxygen analogs of these OP compounds and markedly increased esterase inhibition in SH-SY5Y human neuroblastoma cells. Neither activation system affected cell viability or the activity of AChE or NTE in the absence of OP compounds. Although parathion and chlorpyrifos were activated by RLM, bromine activation required fewer steps and produced more esterase inhibition for a given concentration of chlorpyrifos. However, RLM activation of OP protoxicants produced metabolites other than oxygen analogs and may, therefore, be more relevant as a surrogate for OP biotransformation in vivo. This methodology makes the use of intact cells for in vitro testing of esterase inhibition caused by protoxicant organophosphate compounds a viable alternative to in vivo tests.  (+info)

Anaphylactic bronchoconstriction in BP2 mice: interactions between serotonin and acetylcholine. (3/1796)

1. Immunized BP2 mice developed an acute bronchoconstriction in vivo and airway muscle contraction in vitro in response to ovalbumin (OA) and these contractions were dose dependent. 2. Methysergide or atropine inhibited OA-induced bronchoconstriction in vivo and airway muscle contraction in vitro. 3. Neostigmine potentiated the OA-induced bronchoconstriction in vivo and airway muscle contraction in vitro of BP2 mice. This potentiation was markedly reduced by the administration of methysergide or atropine and when the two antagonists were administered together, the responses were completely inhibited. 4. Neostigmine also potentiated the serotonin (5-HT)- and acetylcholine (ACh)-induced bronchoconstriction and this potentiation was significantly reversed by atropine. 5. These results indicate that OA provokes a bronchoconstriction in immunized BP2 mice by stimulating the release of 5-HT, which in turn acts via the cholinergic mediator, ACh.  (+info)

Efficacy and safety of rivastigmine in patients with Alzheimer's disease: international randomised controlled trial. (4/1796)

OBJECTIVES: To assess the effects of rivastigmine on the core domains of Alzheimer's disease. DESIGN: Prospective, randomised, multicentre, double blind, placebo controlled, parallel group trial. Patients received either placebo, 1-4 mg/day (lower dose) rivastigmine, or 6-12 mg/day (higher dose) rivastigmine. Doses were increased in one of two fixed dose ranges (1-4 mg/day or 6-12 mg/day) over the first 12 weeks with a subsequent assessment period of 14 weeks. SETTING: 45 centres in Europe and North America. PARTICIPANTS: 725 patients with mild to moderately severe probable Alzheimer's disease diagnosed according to the Diagnostic and Statistical Manual of Mental Disorders, fourth edition, and the criteria of the National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer's Disease and Related Disorders Association. OUTCOME MEASURES: Cognitive subscale of the Alzheimer's disease assessment scale, rating on the clinician interview based impression of change incorporating caregiver information scale, and the progressive deterioration scale. RESULTS: At the end of the study cognitive function had deteriorated among those in the placebo group. Scores on the Alzheimer's disease assessment scale improved in patients in the higher dose group when compared with patients taking placebo (P<0.05). Significantly more patients in the higher dose group had improved by 4 points or more than had improved in the placebo group (24% (57/242) v 16% (39/238)). Global function as rated by the clinician interview scale had significantly improved among those in the higher dose group compared with those taking placebo (P<0.001), and significantly more patients in the higher dose group showed improvement than did in the placebo group (37% (80/219) v 20% (46/230)). Mean scores on the progressive deterioration scale improved from baseline in patients in the higher dose group but fell in the placebo group. Adverse events were predominantly gastrointestinal, of mild to moderate severity, transient, and occurred mainly during escalation of the dose. 23% (55/242) of those in the higher dose group, 7% (18/242) of those in the lower dose group, and 7% (16/239) of those in the placebo group discontinued treatment because of adverse events. CONCLUSIONS: Rivastigmine is well tolerated and effective. It improves cognition, participation in activities of daily living, and global evaluation ratings in patients with mild to moderately severe Alzheimer's disease. This is the first treatment to show compelling evidence of efficacy in a predominantly European population.  (+info)

The cholinergic hypothesis of Alzheimer's disease: a review of progress. (5/1796)

Alzheimer's disease is one of the most common causes of mental deterioration in elderly people, accounting for around 50%-60% of the overall cases of dementia among persons over 65 years of age. The past two decades have witnessed a considerable research effort directed towards discovering the cause of Alzheimer's disease with the ultimate hope of developing safe and effective pharmacological treatments. This article examines the existing scientific applicability of the original cholinergic hypothesis of Alzheimer's disease by describing the biochemical and histopathological changes of neurotransmitter markers that occur in the brains of patients with Alzheimer's disease both at postmortem and neurosurgical cerebral biopsy and the behavioural consequences of cholinomimetic drugs and cholinergic lesions. Such studies have resulted in the discovery of an association between a decline in learning and memory, and a deficit in excitatory amino acid (EAA) neurotransmission, together with important roles for the cholinergic system in attentional processing and as a modulator of EAA neurotransmission. Accordingly, although there is presently no "cure" for Alzheimer's disease, a large number of potential therapeutic interventions have emerged that are designed to correct loss of presynaptic cholinergic function. A few of these compounds have confirmed efficacy in delaying the deterioration of symptoms of Alzheimer's disease, a valuable treatment target considering the progressive nature of the disease. Indeed, three compounds have received European approval for the treatment of the cognitive symptoms of Alzheimer's disease, first tacrine and more recently, donepezil and rivastigmine, all of which are cholinesterase inhibitors.  (+info)

Comparison between huperzine A, tacrine, and E2020 on cholinergic transmission at mouse neuromuscular junction in vitro. (6/1796)

AIM: To compare the effects of huperzine A (Hup A), tacrine, and E2020 on cholinergic transmission at mouse neuromuscular junction in vitro. METHODS: The isolated mouse phrenic nerve-hemidiaphragm preparations were used with the conventional intracellular recording technique. The miniature end-plate potentials (MEPP), the mean quantal content of end-plate potentials (EPP), and the resting membrane potentials of muscle fiber were recorded. RESULTS: Hup A, tacrine, and E2020 at the concentration of 1.0 mumol.L-1 increased the amplitude, time-to-peak, and half-decay time of MEPP in the potencies of E2020 > Hup A > tacrine. Hup A did not significantly change the frequency of MEPP, the appearance of giant MEPP or slow MEPP, the resting membrane potentials, and the mean quantal content of EPP. CONCLUSION: Hup A is a selective and potent cholinesterase inhibitor, by which activity it facilitates the cholinergic transmission at mouse neuromuscular junction, and devoid of pre- and post-synaptic actions.  (+info)

Central nervous system-mediated hyperglycemic effects of NIK-247, a cholinesterase inhibitor, and MKC-231, a choline uptake enhancer, in rats. (7/1796)

We investigated the effects of intracerebroventricular administration of NIK-247 (9-amino-2,3,5,6,7,8-hexahydro-1H-cyclo-penta(b)-quinoline monohydrate hydrochloride; a cholinesterase inhibitor) or MKC-231 (2-(2-oxypyrrolidin-1-yl)-N-(2,3-dimethyl-5,6,7,8-tetrahydrofur o[2,3-b]quinolin-4-yl) acetoamide; a choline uptake enhancer) on plasma glucose level in comparison with that of neostigmine administration in rats. The extents of NIK-247- and MKC-231-induced hyperglycemia were considerably less than that by neostigmine, suggesting that the potencies of the drugs to produce the peripheral hyperglycemia may be pharmacologically negligible.  (+info)

Electron paramagnetic resonance reveals altered topography of the active center gorge of acetylcholinesterase after binding of fasciculin to the peripheral site. (8/1796)

Fasciculin, a peptidic toxin from snake venom, inhibits mammalian and fish acetylcholinesterases (AChE) by binding to the peripheral site of the enzyme. This site is located at the rim of a narrow, deep gorge which leads to the active center triad, located at its base. The proposed mechanisms for AChE inhibition by fasciculin include allosteric events resulting in altered conformation of the AChE active center gorge. However, a fasciculin-induced altered topography of the active center gorge has not been directly demonstrated. Using electron paramagnetic resonance with the spin-labeled organophosphate 1-oxyl-2,2,6, 6-tetramethyl-4-piperidinylethylphosphorofluoridate (EtOSL) specifically bound to the catalytic serine of mouse AChE (mAChE), we show that bound fasciculin on mAChE slows down, but does not prevent phosphorylation of the active site serine by EtOSL and protects the gorge conformation against thermal denaturation. Most importantly, a restricted freedom of motion of the spin label bound to the fasciculin-associated mAChE, compared to mAChE, is evidenced. Molecular models of mAChE and fasciculin-associated mAChE with tethered EtOSL enantiomers indicate that this restricted motion is due to greater proximity of the S-EtOSL nitroxide radical to the W86 residue in the fasciculin-associated enzyme. Our results demonstrate a topographical alteration indicative of a restricted conformation of the active center gorge of mAChE with bound fasciculin at its rim.  (+info)

The symptoms of Alzheimer's disease can vary from person to person and may progress slowly over time. Early symptoms may include memory loss, confusion, and difficulty with problem-solving. As the disease progresses, individuals may experience language difficulties, visual hallucinations, and changes in mood and behavior.

There is currently no cure for Alzheimer's disease, but there are several medications and therapies that can help manage its symptoms and slow its progression. These include cholinesterase inhibitors, memantine, and non-pharmacological interventions such as cognitive training and behavioral therapy.

Alzheimer's disease is a significant public health concern, affecting an estimated 5.8 million Americans in 2020. It is the sixth leading cause of death in the United States, and its prevalence is expected to continue to increase as the population ages.

There is ongoing research into the causes and potential treatments for Alzheimer's disease, including studies into the role of inflammation, oxidative stress, and the immune system. Other areas of research include the development of biomarkers for early detection and the use of advanced imaging techniques to monitor progression of the disease.

Overall, Alzheimer's disease is a complex and multifactorial disorder that poses significant challenges for individuals, families, and healthcare systems. However, with ongoing research and advances in medical technology, there is hope for improving diagnosis and treatment options in the future.

There are several types of dementia, each with its own set of symptoms and characteristics. Some common types of dementia include:

* Alzheimer's disease: This is the most common form of dementia, accounting for 50-70% of all cases. It is a progressive disease that causes the death of brain cells, leading to memory loss and cognitive decline.
* Vascular dementia: This type of dementia is caused by problems with blood flow to the brain, often as a result of a stroke or small vessel disease. It can cause difficulty with communication, language, and visual-spatial skills.
* Lewy body dementia: This type of dementia is characterized by the presence of abnormal protein deposits called Lewy bodies in the brain. It can cause a range of symptoms, including memory loss, confusion, hallucinations, and difficulty with movement.
* Frontotemporal dementia: This is a group of diseases that affect the front and temporal lobes of the brain, leading to changes in personality, behavior, and language.

The symptoms of dementia can vary depending on the underlying cause, but common symptoms include:

* Memory loss: Difficulty remembering recent events or learning new information.
* Communication and language difficulties: Struggling to find the right words or understand what others are saying.
* Disorientation: Getting lost in familiar places or having difficulty understanding the time and date.
* Difficulty with problem-solving: Trouble with planning, organizing, and decision-making.
* Mood changes: Depression, anxiety, agitation, or aggression.
* Personality changes: Becoming passive, suspicious, or withdrawn.
* Difficulty with movement: Trouble with coordination, balance, or using utensils.
* Hallucinations: Seeing or hearing things that are not there.
* Sleep disturbances: Having trouble falling asleep or staying asleep.

The symptoms of dementia can be subtle at first and may progress slowly over time. In the early stages, they may be barely noticeable, but as the disease progresses, they can become more pronounced and interfere with daily life. It is important to seek medical advice if you or a loved one is experiencing any of these symptoms, as early diagnosis and treatment can help improve outcomes.

The different types of Neurotoxicity Syndromes include:

1. Organophosphate-induced neurotoxicity: This syndrome is caused by exposure to organophosphate pesticides, which can damage the nervous system and cause symptoms such as headaches, dizziness, and memory loss.
2. Heavy metal neurotoxicity: Exposure to heavy metals, such as lead, mercury, and arsenic, can damage the nervous system and cause symptoms such as tremors, muscle weakness, and cognitive impairment.
3. Pesticide-induced neurotoxicity: This syndrome is caused by exposure to pesticides, which can damage the nervous system and cause symptoms such as headaches, dizziness, and memory loss.
4. Solvent-induced neurotoxicity: Exposure to solvents, such as toluene and benzene, can damage the nervous system and cause symptoms such as memory loss, difficulty with concentration, and mood changes.
5. Medication-induced neurotoxicity: Certain medications, such as antidepressants and antipsychotics, can damage the nervous system and cause symptoms such as tremors, muscle rigidity, and cognitive impairment.
6. Environmental neurotoxicity: Exposure to environmental toxins, such as air pollution and pesticides, can damage the nervous system and cause symptoms such as headaches, dizziness, and memory loss.
7. Neurodegenerative disease-induced neurotoxicity: Neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease, can cause neurotoxicity and lead to symptoms such as cognitive decline, memory loss, and motor dysfunction.
8. Traumatic brain injury-induced neurotoxicity: Traumatic brain injury can cause neurotoxicity and lead to symptoms such as cognitive impairment, memory loss, and mood changes.
9. Stroke-induced neurotoxicity: A stroke can cause neurotoxicity and lead to symptoms such as weakness or paralysis on one side of the body, difficulty with speech and language, and memory loss.
10. Neurodevelopmental disorder-induced neurotoxicity: Neurodevelopmental disorders, such as autism spectrum disorder, can cause neurotoxicity and lead to symptoms such as cognitive impairment, social withdrawal, and repetitive behaviors.

It is important to note that these are just a few examples of the many different types of neurotoxicity that can occur, and that each type may have its own unique set of causes, symptoms, and treatments. If you suspect that you or someone you know may be experiencing neurotoxicity, it is important to seek medical attention as soon as possible in order to receive an accurate diagnosis and appropriate treatment.

The symptoms of Lewy body disease can vary from person to person, but they often include:

1. Cognitive problems, such as difficulty with memory, attention, and decision-making.
2. Slowness of movement, rigidity, and tremors, similar to those seen in Parkinson's disease.
3. Visual hallucinations and sleep disturbances.
4. Balance problems and falls.
5. Mood changes, such as depression and anxiety.

Lewy body disease can be difficult to diagnose, as it can resemble other conditions such as Alzheimer's disease or Parkinson's disease. A definitive diagnosis is usually made through an autopsy after death, but a clinical diagnosis can be made based on a combination of symptoms and medical imaging studies.

There is no cure for Lewy body disease, but medications and therapies can help manage its symptoms. Treatment options may include cholinesterase inhibitors, dopamine agonists, and antidepressants, as well as physical, occupational, and speech therapy. In some cases, surgery may be recommended to regulate medication or improve cognitive function.

Lewy body disease is a relatively rare condition, affecting about 1% of people over the age of 65. It is more common in men than women, and the risk of developing the disease increases with age. There is currently no known cause for Lewy body disease, but research suggests that it may be linked to genetic factors and exposure to certain environmental toxins.

In summary, Lewy body disease is a progressive neurodegenerative disorder that affects the brain and nervous system, characterized by abnormal protein deposits called Lewy bodies. It can cause a range of cognitive and motor symptoms, and diagnosis can be challenging. There is no cure for the disease, but medications and therapies can help manage its symptoms.

The symptoms of organophosphate poisoning can vary depending on the severity of exposure and individual sensitivity, but may include:

1. Respiratory problems: Difficulty breathing, wheezing, coughing, and shortness of breath
2. Nervous system effects: Headache, dizziness, confusion, tremors, and muscle weakness
3. Eye irritation: Redness, itching, tearing, and blurred vision
4. Skin irritation: Redness, itching, and burns
5. Gastrointestinal effects: Nausea, vomiting, diarrhea, and abdominal pain
6. Cardiovascular effects: Rapid heart rate, low blood pressure, and cardiac arrhythmias
7. Neurological effects: Seizures, coma, and memory loss

Organophosphate poisoning can be caused by ingestion of contaminated food or water, inhalation of pesticides, or absorption through the skin. Treatment typically involves supportive care, such as fluids and oxygen, as well as medications to counteract the effects of organophosphates on the nervous system. In severe cases, hospitalization may be necessary to monitor and treat the patient.

Prevention is key in avoiding organophosphate poisoning, which can be achieved by using protective clothing and equipment when handling pesticides, keeping products away from food and children, and following the recommended dosage and application instructions carefully. Regular testing of soil and water for organophosphate residues can also help prevent exposure.

In conclusion, organophosphate poisoning is a serious health hazard that can result from exposure to pesticides and insecticides. Prompt recognition of symptoms and proper treatment are essential in preventing long-term health effects and reducing the risk of fatalities. Prevention through safe handling practices and regular testing of soil and water for organophosphate residues can also help minimize the risks associated with these chemicals.

* Heart block: A condition where the electrical signals that control the heart's rhythm are blocked or delayed, leading to a slow heart rate.
* Sinus node dysfunction: A condition where the sinus node, which is responsible for setting the heart's rhythm, is not functioning properly, leading to a slow heart rate.
* Medications: Certain medications, such as beta blockers, can slow down the heart rate.
* Heart failure: In severe cases of heart failure, the heart may become so weak that it cannot pump blood effectively, leading to a slow heart rate.
* Electrolyte imbalance: An imbalance of electrolytes, such as potassium or magnesium, can affect the heart's ability to function properly and cause a slow heart rate.
* Other medical conditions: Certain medical conditions, such as hypothyroidism (an underactive thyroid) or anemia, can cause bradycardia.

Bradycardia can cause symptoms such as:

* Fatigue
* Weakness
* Dizziness or lightheadedness
* Shortness of breath
* Chest pain or discomfort

In some cases, bradycardia may not cause any noticeable symptoms at all.

If you suspect you have bradycardia, it is important to consult with a healthcare professional for proper diagnosis and treatment. They may perform tests such as an electrocardiogram (ECG) or stress test to determine the cause of your slow heart rate and develop an appropriate treatment plan. Treatment options for bradycardia may include:

* Medications: Such as atropine or digoxin, to increase the heart rate.
* Pacemakers: A small device that is implanted in the chest to help regulate the heart's rhythm and increase the heart rate.
* Cardiac resynchronization therapy (CRT): A procedure that involves implanting a device that helps both ventricles of the heart beat together, improving the heart's pumping function.

It is important to note that bradycardia can be a symptom of an underlying condition, so it is important to address the underlying cause in order to effectively treat the bradycardia.

The symptoms of vascular dementia can vary depending on the location and severity of the damage to the brain, but common symptoms include:

* Memory loss, such as difficulty remembering recent events or learning new information
* Confusion and disorientation
* Difficulty with communication, including trouble finding the right words or understanding what others are saying
* Difficulty with problem-solving, decision-making, and judgment
* Mood changes, such as depression, anxiety, or agitation
* Personality changes, such as becoming more passive or suspicious
* Difficulty with coordination and movement, including trouble walking or balance

Vascular dementia can be caused by a variety of conditions that affect the blood vessels in the brain, including:

* Stroke or transient ischemic attack (TIA, or "mini-stroke")
* Small vessel disease, such as tiny strokes or changes in the blood vessels that occur over time
* Moyamoya disease, a rare condition caused by narrowing or blockage of the internal carotid artery and its branches
* Cerebral amyloid angiopathy, a condition in which abnormal protein deposits build up in the blood vessels of the brain
* Other conditions that can cause reduced blood flow to the brain, such as high blood pressure, diabetes, or cardiovascular disease

There is no cure for vascular dementia, but there are several treatment options available to help manage its symptoms and slow its progression. These may include medications to improve memory and cognitive function, physical therapy to maintain mobility and strength, and lifestyle changes such as a healthy diet and regular exercise. In some cases, surgery or endovascular procedures may be recommended to treat the underlying cause of the dementia, such as a stroke or blocked blood vessel.

It is important for individuals with vascular dementia to receive timely and accurate diagnosis and treatment, as well as ongoing support and care from healthcare professionals, family members, and caregivers. With appropriate management, many people with vascular dementia are able to maintain their independence and quality of life for as long as possible.

Types of Cognition Disorders: There are several types of cognitive disorders that affect different aspects of cognitive functioning. Some common types include:

1. Attention Deficit Hyperactivity Disorder (ADHD): Characterized by symptoms of inattention, hyperactivity, and impulsivity.
2. Traumatic Brain Injury (TBI): Caused by a blow or jolt to the head that disrupts brain function, resulting in cognitive, emotional, and behavioral changes.
3. Alzheimer's Disease: A progressive neurodegenerative disorder characterized by memory loss, confusion, and difficulty with communication.
4. Stroke: A condition where blood flow to the brain is interrupted, leading to cognitive impairment and other symptoms.
5. Parkinson's Disease: A neurodegenerative disorder that affects movement, balance, and cognition.
6. Huntington's Disease: An inherited disorder that causes progressive damage to the brain, leading to cognitive decline and other symptoms.
7. Frontotemporal Dementia (FTD): A group of neurodegenerative disorders characterized by changes in personality, behavior, and language.
8. Post-Traumatic Stress Disorder (PTSD): A condition that develops after a traumatic event, characterized by symptoms such as anxiety, avoidance, and hypervigilance.
9. Mild Cognitive Impairment (MCI): A condition characterized by memory loss and other cognitive symptoms that are more severe than normal age-related changes but not severe enough to interfere with daily life.

Causes and Risk Factors: The causes of cognition disorders can vary depending on the specific disorder, but some common risk factors include:

1. Genetics: Many cognitive disorders have a genetic component, such as Alzheimer's disease, Parkinson's disease, and Huntington's disease.
2. Age: As people age, their risk of developing cognitive disorders increases, such as Alzheimer's disease, vascular dementia, and frontotemporal dementia.
3. Lifestyle factors: Factors such as physical inactivity, smoking, and poor diet can increase the risk of cognitive decline and dementia.
4. Traumatic brain injury: A severe blow to the head or a traumatic brain injury can increase the risk of developing cognitive disorders, such as chronic traumatic encephalopathy (CTE).
5. Infections: Certain infections, such as meningitis and encephalitis, can cause cognitive disorders if they damage the brain tissue.
6. Stroke or other cardiovascular conditions: A stroke or other cardiovascular conditions can cause cognitive disorders by damaging the blood vessels in the brain.
7. Chronic substance abuse: Long-term use of drugs or alcohol can damage the brain and increase the risk of cognitive disorders, such as dementia.
8. Sleep disorders: Sleep disorders, such as sleep apnea, can increase the risk of cognitive disorders, such as dementia.
9. Depression and anxiety: Mental health conditions, such as depression and anxiety, can increase the risk of cognitive decline and dementia.
10. Environmental factors: Exposure to certain environmental toxins, such as pesticides and heavy metals, has been linked to an increased risk of cognitive disorders.

It's important to note that not everyone with these risk factors will develop a cognitive disorder, and some people without any known risk factors can still develop a cognitive disorder. If you have concerns about your cognitive health, it's important to speak with a healthcare professional for proper evaluation and diagnosis.

Cholinesterase inhibitors (ChEIs), also known as anti-cholinesterase, are chemicals that prevent the breakdown of the ... Cholinesterase inhibitors came to a public attention in 2020 when Russian opposition and dissent figure Alexei Navalny was ... "Cholinesterase Inhibitors (Medical Use & WMD)". PharmWiki. Tulane University School of Medicine. Retrieved 24 August 2020. ... Meng, Yan‑Hong; Wang, Pan‑Pan; Song, Ya‑Xue; Wang, Jian‑Hua (2019-03-01). "Cholinesterase inhibitors and memantine for ...
The use of medications for treatment of Alzheimer's dementia, such as cholinesterase inhibitors and memantine, has shown small[ ... cholinesterase inhibitors galantamine, donepezil, rivastigmine; Studies have been proposed to evaluate whether an extract of ... These medications include angiotensin converting enzyme inhibitors, diuretics, calcium channel blockers, sympathetic nerve ... inhibitors, angiotensin II receptor antagonists or adrenergic antagonists. Elevated lipid levels, including HDL, were found to ...
Rodda J, Morgan S, Walker Z (October 2009). "Are cholinesterase inhibitors effective in the management of the behavioral and ... Birks J (January 2006). Birks JS (ed.). "Cholinesterase inhibitors for Alzheimer's disease". The Cochrane Database of ... March 2008). "Effectiveness of cholinesterase inhibitors and memantine for treating dementia: evidence review for a clinical ... "Syncope and its consequences in patients with dementia receiving cholinesterase inhibitors: a population-based cohort study". ...
Birks, J. (2006). Birks, Jacqueline S (ed.). "Cholinesterase inhibitors for Alzheimer's disease". The Cochrane Database of ...
As with other cholinesterase inhibitors, galantamine may not be effective for treating mild cognitive impairment. The FDA ... Galantamine also works as a weak competitive and reversible cholinesterase inhibitor in all areas of the body. By inhibiting ... In practice, some other cholinesterase inhibitors might be better tolerated; however, a careful and gradual titration over more ... Galantamine's side effect profile was similar to that of other cholinesterase inhibitors, with gastrointestinal symptoms being ...
Birks, J. (2006). Birks, Jacqueline S (ed.). "Cholinesterase inhibitors for Alzheimer's disease". The Cochrane Database of ...
Birks, J. (2006). Birks, Jacqueline S (ed.). "Cholinesterase inhibitors for Alzheimer's disease". The Cochrane Database of ...
January 1967). "Selenophosphorus Compounds as Powerful Cholinesterase Inhibitors". Journal of Medicinal Chemistry. 10 (1): 115- ... Selenophos is an extremely potent organophosphate acetylcholinesterase inhibitor. It is the selenium analog of the VE nerve ... Acetylcholinesterase inhibitors, Organoselenium compounds, Ethyl esters, Diethylamino compounds, All stub articles, Organic ...
Cholinesterase inhibitor Nicotinic antagonist FULTON, MP; MOGEY, GA (June 1954). "Some selective inhibitors of true ... Olivera-Bravo, S; Ivorra, I; Morales, A (January 2005). "The acetylcholinesterase inhibitor BW284c51 is a potent blocker of ... BW284C51 is a selective acetylcholinesterase inhibitor. It is also a nicotinic antagonist. ... Acetylcholinesterase inhibitors, Quaternary ammonium compounds, Ketones, Allyl compounds, Bromides, Bisquaternary ...
Sharma K (August 2019). "Cholinesterase inhibitors as Alzheimer's therapeutics (Review)". Molecular Medicine Reports. 20 (2): ... "Phenserine - Next Generation AChE Inhibitor". Clinical Trials Arena. Retrieved 2020-04-06. Becker RE, Kapogiannis D, Greig NH ( ... Phenserine was introduced as an inhibitor of acetylcholinesterase (AChE) and demonstrated significant alleviation in numerous ... Phenserine serves as an acetylcholinesterase (AChE) inhibitor which selectively acts on the acetylcholinesterase enzyme. It ...
Historical development of organophosphorus cholinesterase inhibitors." Handbook of Experimental Pharmacology.". Cholinesterases ... doi:10.1007/978-3-642-68441-8. ISBN 978-3-642-68443-2. S2CID 33095322.The history of cholinesterase inhibitors: who was ... Petroianu, Georg (2015). "History of organophosphorus cholinesterase inhibitors & reactivators". Military Medical Science ... TEPP was discovered to be an inhibitor of cholinesterases. Schrader referred to the studies by Eberhard Gross, who was the ...
Walker LC, Rosen RF (2006). "Alzheimer therapeutics-what after the cholinesterase inhibitors?". Age Ageing. 35 (4): 332-335. ...
"Cholinesterase Inhibitors - Organophosphate-Induced Delayed Neuropathy (OPIDN)". ATSDR - Environmental Medicine & Environmental ...
It produces illness typical of cholinesterase inhibitors. Vomiting, nausea, diarrhea and excessive salivation are some common ... Organophosphates are acetylcholinesterase inhibitors and disrupt the signal transduction at the cholinergic synapse. It is ... There were no effects reported on plasma or red blood cell cholinesterase activity. These results were insufficient to ... Carbophenothion affects the nervous system by inhibiting cholinesterase. There are no signs of chronic or carcinogenic effects ...
Like other cholinesterase inhibitors, it requires doses to be increased gradually over several weeks; this is usually referred ... Rivastigmine (sold under the trade name Exelon among others) is a cholinesterase inhibitor used for the treatment of mild to ... Ali TB, Schleret TR, Reilly BM, Chen WY, Abagyan R (2015). "Adverse Effects of Cholinesterase Inhibitors in Dementia, According ... Rivastigmine, a cholinesterase inhibitor, inhibits both butyrylcholinesterase and acetylcholinesterase (unlike donepezil, which ...
Walker LC, Rosen RF (Jul 2006). "Alzheimer therapeutics-what after the cholinesterase inhibitors?". Age and Ageing. 35 (4): 332 ... Another BACE1 inhibitor that has reached phase II trials is the Eli Lilly's inhibitor LY2886721. The data on phase I trial were ... "CoMentis BACE Inhibitor Debuts". April 2008. "Merck Presents Results of a Phase I Clinical Trial Evaluating Investigational ... The BACE1 expression is influenced by the inflammatory state: during AD the cytokines reduce the PPAR1 an inhibitor of BACE1 ...
It is a cholinesterase inhibitor. Breakdown in soil is 6.1 days in sand, 309 days in water at pH 5.0, 27 days at pH 7.0, and 3 ... Acetylcholinesterase inhibitors, Organophosphate insecticides, Phosphoramidothioates, Methoxy compounds). ...
It is a cholinesterase inhibitor. When heated to decomposition, it emits toxic fumes of sulfur oxides and phosphorus oxides. A ... Symptoms of exposure to this type of compound include cholinesterase inhibition, miosis, frontal headache, increased bronchial ...
Cholinesterase Inhibitors & Other Pharmacologic Antagonists to Neuromuscular Blocking Agents.". Morgan & Mikhail's Clinical ... reverse-transcriptase inhibitors targeting HIV/AIDS, neuraminidase inhibitors targeting influenza, and terminase inhibitors ... For example, an inhibitor might compete with substrate A for the first binding site, but be a non-competitive inhibitor with ... New inhibitors are used to obtain crystallographic structures of the enzyme in an inhibitor/enzyme complex to show how the ...
... a non-specific cholinesterase inhibitor; ammosamide B (V), a cytotoxic natural product that targets myosin; lavendustin A (VI ... Pommier, Yves; Cushman, Mark; Doroshow, James H. (2018-12-18). "Novel clinical indenoisoquinoline topoisomerase I inhibitors: a ... Polymerase-1 Inhibitors from the Modification of Indeno[1,2-c]isoquinolinone". Journal of Medicinal Chemistry. 48 (16): 5100- ... a tyrosine kinase inhibitor; and (+)- and (-)-corynoline. Professor Cushman has received various awards including: Purdue ...
It acts as a cholinesterase inhibitor. The commercial product typically exists as a mixture of 70% (Z)-isomer and 30% (E)- ... He collapsed and exhibited significant depression of serum cholinesterase, but recovered completely within 2 days after ... Acetylcholinesterase inhibitors, Organophosphate insecticides, Carboxamides, Organochlorides, Methyl esters). ...
Strength may improve with administration of cholinesterase inhibitors.[citation needed] Berger, in 1876, first reported a case ...
Acetylcholinesterase inhibitors are one of two types of cholinesterase inhibitors; the other being butyryl-cholinesterase ... Acetylcholinesterase inhibitors (AChEIs) also often called cholinesterase inhibitors, inhibit the enzyme acetylcholinesterase ... Inhibitors like TEPP modify the serine residue in the esteratic site of the cholinesterase. This phosphorylation inhibits the ... Administration of reversible cholinesterase inhibitors is contraindicated with those that have urinary retention due to ...
Tammelin, Lars-Erik (1958). Choline esters: substrate and inhibitors of cholinesterases. Stockholm. SELIBR 9470776. Vem är det ... Honorary Doctor of Medicine (1973) Tammelin, Lars-Erik (1958). Choline esters: substrate and inhibitors of cholinesterases. ... linked to their chemical similarity to the neurotransmitter acetylcholine and their ability to block the enzyme cholinesterase ...
... which is a less potent AChE inhibitor. Soman can also bind to other esterases, e.g., AChE, cholinesterase (ChE) and ... interfering with normal functioning of the mammalian nervous system by inhibiting the enzyme cholinesterase. It is an inhibitor ... "Behavioral Changes in the Rat after Low Doses of Cholinesterase Inhibitors". Toxicological Sciences. 4 (2part2): 195-208. doi: ... AChE inhibitors and substrates in Proteopedia 2wfz in Proteopedia 2wg0 in Proteopedia 2wg1 in Proteopedia 1som in Proteopedia ...
Acetylcholinesterase inhibitor Nerve agent "Cholinesterase Reactivators - MeSH - NCBI". www.ncbi.nlm.nih.gov. Antonijevic, B.; ... Cholinesterase reactivators are drugs that reverses the inhibition of cholinesterase by organophosphates or sulfonates. They ... v t e v t e (Cholinesterase reactivators, All stub articles, Pharmacology stubs, Toxicology stubs). ...
Contribution to the study of the mechanism of action of cholinesterase inhibitors. J. Pharmacol. Exp. Therap. 101: 327-343. ... Ontogenesis of cholinesterases. In: Cholinesterases and Anticholinesterase Agents, G. B. Koelle, Ed., pp. 129 - 186, Handbch. d ... In: Cholinesterases and Anticholinesterase Agents, G. B. Koelle, Ed., pp. 799 -832, Handbch. d. Exper. Pharmakol., Erganzungswk ... Histochemical studies of cholinesterases in Ciona intestinalis. Comp. Biochem. Physiol. 17: 553-558. "ASPET , Obituary: ...
Boxwood [Database] 2015 03-13-2015 [cited 2016 03-01-2016]. Orhan, I.E., et al., Selective cholinesterase inhibitors from Buxus ... McGleenon, B.M., K.B. Dynan, and A.P. Passmore, Acetylcholinesterase inhibitors in Alzheimer's disease. British Journal of ... Murray, A.P., et al., Natural AChE Inhibitors from Plants and their Contribution to Alzheimer's Disease Therapy. Current ... Cyclobuxine could also have a positive effect on Alzheimer's disease, as acetylcholinesterase inhibitors are an important ...
Myasthenia is treated with immunosuppressants, cholinesterase inhibitors and, in selected cases, thymectomy. Demyelination is ...
RIC-3 also known as resistance to inhibitors of cholinesterase 3 is a chaperone protein that in humans is encoded by the RIC3 ... "Entrez Gene: RIC3 resistance to inhibitors of cholinesterase 3 homolog (C. elegans)". Williams ME, Burton B, Urrutia A, et al ... Nguyen M, Alfonso A, Johnson CD, Rand JB (Jun 1995). "Caenorhabditis elegans mutants resistant to inhibitors of ...
It also acts as a histamine N-methyltransferase inhibitor. Tacrine was the prototypical cholinesterase inhibitor for the ... It was the first centrally acting cholinesterase inhibitor approved for the treatment of Alzheimer's disease, and was marketed ... Tacrine is a centrally acting acetylcholinesterase inhibitor and indirect cholinergic agonist (parasympathomimetic). ...
... e is also a cholinesterase inhibitor and a neurotoxin. A study was conducted to investigate the effect of ...
ALDRIDGE, WN; DAVISON, AN (December 1952). "The inhibition of erythrocyte cholinesterase by tri-esters of phosphoric acid. II. ... Parathion S is a potent acetylcholinesterase inhibitor. Paraoxon Parathion Diisopropyl paraoxon Ro 3-0419 Ro 3-0422 "ChemIDplus ... Acetylcholinesterase inhibitors, Organothiophosphate esters, Ethyl esters, Nitrobenzenes, All stub articles, Organic compound ... ". DIGGLE, WM; GAGE, JC (September 1951). "Cholinesterase inhibition in vitro by OO-diethyl O-p-nitrophenyl thiophosphate ( ...
It is a corrosive, and as a cholinesterase inhibitor, highly toxic through dermal absorption. The molecule is tetrahedral. The ...
UV protectants and specific inhibitors of enzymes. Cyanotoxins are often implicated in what are commonly called red tides or ... because it is not degraded by cholinesterase which normally performs this function. As a result, the muscle cells contract ...
... is an extremely potent acetylcholinesterase inhibitor. As a transition state analog of acetylcholinesterase, TMTFA is ... Exploiting protein fluctuations at the active-site gorge of human cholinesterases: further optimization of the design strategy ... Acetylcholinesterase inhibitor Methylfluorophosphonylcholine Transition state analog Brodbeck, U.; Schweikert, K.; Gentinetta, ... a femtomolar inhibitor of acetylcholinesterase". Journal of the American Chemical Society. 115 (22): 9939-9941. doi:10.1021/ ...
... cholinesterase inhibitors), and other substances (sugar-free mints, nicotinamide). Medications which stimulate saliva ...
... in patients with mild-to-moderate Alzheimer's disease stable on cholinesterase inhibitors or memantine-A randomized, double- ...
Biochemical investigation of cholinesterases and carboxylesterases from the cotton bollworm Heliothis armigera. Chem Nat Compd ... Acetylcholinesterase inhibitors, Ethyl esters, Thioethers, All stub articles, Organic compound stubs). ... "Biochemical investigation of cholinesterases and carboxylesterases from the cotton bollworm Heliothis armigera". Chemistry of ...
Some populations of R. microplus have developed resistance to acetylcholinesterase inhibitors. The search for the ... "Natural genomic amplification of cholinesterase genes in animals". Journal of Neurochemistry. International Society for ...
... is a cholinesterase inhibitor used as an insecticide and avicide; for example, against rice stem borers and house ... Acetylcholinesterase inhibitors, Organophosphate insecticides, Nitriles, Organothiophosphate esters). ...
... , like other cholinesterase inhibitors, can cause nightmares due to enhanced activation of the visual association ... Donepezil along with other cholinesterase inhibitors is suggested as having potential for trouble behaviors, irritability, ... the effects of donepezil and other drugs that act as cholinesterase inhibitors could thus be effective in the treatment of the ... In addition to its actions as an acetylcholinesterase inhibitor, donepezil has been found to act as a potent agonist of the σ1 ...
With higher exposures, however, naled can cause cholinesterase inhibition in humans, which in turn can overstimulate the ... Acetylcholinesterase inhibitors, Organophosphate insecticides, Organochlorides, Methyl esters, Organobromides). ... Persons who work closely with naled or other organophosphate pesticides should undergo regular testing of their cholinesterase ...
Isolation and synthesis of a new cholinesterase inhibitor from Nostoc 78-12A". Journal of Natural Products. 68 (12): 1793-5. ...
Calabar bean contains physostigmine, a reversible cholinesterase inhibitor alkaloid. The alkaloid physostigmine acts in effect ... "Acetylcholinesterase Inhibitors: Pharmacology and Toxicology". Current Neuropharmacology. 11 (3): 315-335. doi:10.2174/ ...
... cholinesterase inhibitor; not allowed in WA Thiophanate-methyl (fungicide): Carcinogen; Not allowed in WA or CO, found on ...
... some patients have been successfully treated with cholinesterase inhibitors, such as physostigmine or neostigmine, but success ...
Bellet, Eugene M.; Casida, John E. (Dec 14, 1973). "Bicyclic Phosphorus Esters: High Toxicity without Cholinesterase Inhibition ... essentially stopping it from functioning properly as an inhibitor in the cerebellum. In-depth, the normal binding mechanism for ...
... aromatase inhibitors MeSH D27.505.519.389.200 - carbonic anhydrase inhibitors MeSH D27.505.519.389.275 - cholinesterase ... cholinesterase inhibitors MeSH D27.505.519.625.120.400 - cholinesterase reactivators MeSH D27.505.519.625.150 - dopamine agents ... cholinesterase inhibitors MeSH D27.505.696.577.120.400 - cholinesterase reactivators MeSH D27.505.696.577.150 - dopamine agents ... trypsin inhibitors MeSH D27.505.519.389.755 - protein kinase inhibitors MeSH D27.505.519.389.760 - protein synthesis inhibitors ...
It covalently binds by its phosphate group to serine group at the active site of the cholinesterase. Once bound, the enzyme is ... Echothiophate (Phospholine) is an irreversible acetylcholinesterase inhibitor. It is used as an ocular antihypertensive in the ... Because of the very slow rate at which echothiophate is hydrolyzed by cholinesterase, its effects can last a week or more. ... Acetylcholinesterase inhibitors, Organothiophosphate esters, Ophthalmology drugs, Iodides, Phosphorylthiocholines). ...
Cholinesterase is an enzyme that causes the hydrolysis of acetylcholine, an excitatory neurotransmitter that is abundant in the ... AChE inhibitors are either reversible or irreversible, and carbamates are safer than organophosphorus insecticides, which are ... Certain pesticides, such as organophosphates, neonicotinoids, and carbamates, react via cholinesterase inhibition. ...
Galli A, Ranaudo E, Giannini L, Costagli C (November 1996). "Reversible inhibition of cholinesterases by opioids: possible ... It is a metabolite of the acetylcholinesterase inhibitor physostigmine but unlike physostigmine, the acetylcholinesterase ...
... cholinesterase inhibitors [donepezil, rivastigmine]), SSRIs (fluoxetine, sertraline), serotonin-norepinephrine-reuptake ... Proton pump inhibitors (PPIs) were found to be better than placebo in a literature review, especially when looking at long-term ... It is often treated with proton pump inhibitors. If left untreated, the chronic damage to the esophageal tissues poses a risk ... "Proton Pump Inhibitors: Use in Adults" (PDF). Centers for Medicare & Medicaid Services. 2015. Retrieved 2022-01-27. Heiran, ...
This Initial Check will help you assess your current knowledge and skill level about cholinesterase inhibitors. To take the ... While laboratory tests can be used to estimate the exposure to cholinesterase inhibitors (cholinesterase levels and direct ... and Serum Cholinesterase and Direct Measurement of Cholinesterase Inhibitors and Their Metabolic Byproducts. ... This Initial Check will help you assess your current knowledge and skill level about cholinesterase inhibitors. To take the ...
Atropine Dosing for Cholinesterase Inhibitor Toxicity doses atropine for cholinesterase inhibitor toxicity (prescribed drugs, ... Atropine Dosing for Cholinesterase Inhibitor Toxicity. Doses atropine for cholinesterase inhibitor toxicity (prescribed drugs, ...
Results of search for su:{Cholinesterase inhibitors} Refine your search. *. Availability. * Limit to currently available ...
A Meeting on the topic "Latest Developments in Dementia - Alzheimers Disease: From Cholinesterase Inhibitors to Stem Cell ... Latest Developments in Dementia 2008, Alzheimers Disease: From Cholinesterase Inhibitors to Stem Cell Treatment. King George ...
Cholinesterase Inhibitors (Donepezil, Rivastigmine, Galantamine). Cholinesterase inhibitors are designed to protect the ... Cholinesterase inhibitors (generally used to treat mild-to-moderate AD; donepezil is also approved for treatment of severe ... Cholinesterase inhibitors are used to treat mild-to-moderate stages of the disease.) By blocking NMDA receptors, memantine ... Cholinesterase inhibitors may increase the risk for gastrointestinal bleeding or ulcers, largely when used with NSAIDs (which ...
Cholinesterase inhibitors with pyrethrin or pyrethroid only. Cholinesterase inhibitors plus pyrethrin or pyrethroid plus other ... Cholinesterase inhibitors plus organochlorine compounds. Cholinesterase inhibitors with compounds not otherwise listed. ...
Cholinesterase Inhibitors. Enzyme Inhibitors. Molecular Mechanisms of Pharmacological Action. Cholinergic Agents. ... a novel phosphodiesterase type 9 inhibitor, in two randomised controlled phase II studies in patients with prodromal and mild ...
Cholinesterase Inhibitors / pharmacology * Cholinesterase Inhibitors / therapeutic use * Drugs, Chinese Herbal / pharmacology * ...
Cholinesterase inhibitors Pregnancy Category. C - Risk cannot be ruled out CSA Schedule. Not a controlled drug Labeler / ... Galantamine is used in the treatment of alzheimers disease and belongs to the drug class cholinesterase inhibitors. Risk ...
Myasthenia Gravis (MG) Treatment Market Size, Share & Trends Analysis, By Drug Class (Cholinesterase Inhibitors, ... Cholinesterase Inhibitors, Corticosteroids, Immunosuppressants, IVIg, Monoclonal Antibodies. By Distribution Channel. Hospital ... Myasthenia Gravis (MG) Treatment Market Size, Share & Trends Analysis, By Drug Class (Cholinesterase Inhibitors, ... It is divided into several categories, including By Drug Class (Cholinesterase Inhibitors, Corticosteroids, Immunosuppressants ...
Acute (12 h), short-term (4 days) or chronic (7-18 days) treatment with the cholinesterase inhibitors neostigmine (0.1 mg/kg), ... Acute and chronic effects of cholinesterase inhibitors and pilocarpine on the density and sensitivity of central and peripheral ... Acute and chronic effects of cholinesterase inhibitors and pilocarpine on the density and ...
This study aimed to develop simple colorimetric test to detect cholinesterase inhibitors in the gastric content, using ... Simple colorimetric method for cholinesterase-inhibitor screening in gastric content by using phytoesterase enzyme from kidney ... Background and Objective: Diagnosis of cholinesterase inhibitor insecticide ingestion is based on clinical suspicious and ... The inhibitor concentrations measured by the developed phytoesterase enzyme inhibition assay were compared with those analyzed ...
NIOSH-Publication; NIOSH-Author; HHE-72-46-29; Region-2; Hazards-Confirmed; Pesticides; Enzyme-inhibitors; Cholinesterase- ... Recommendations include monitoring of pre- exposure cholinesterase levels, checking of red blood cell or plasma decrease, ... Data are given for cholinesterase (9001085) levels of affected persons, symptoms, and details of dermatitis resulting from the ... inhibitors; Environmental-contaminants; Organo-phosphorus-insecticides; Biochemical-reactions; Skin-disorders; Systemic- ...
Rivastigmine belongs to a family of medications known as cholinesterase inhibitors. It is used to treat symptoms of mild-to- ... Rivastigmine belongs to a family of medications known as cholinesterase inhibitors. It is used to treat symptoms of mild-to- ... sphingosine 1-phosphate receptor (S1P) receptor inhibitors (e.g., fingolimod, ozanimod, ponesimod, siponimod) ...
Behavioral and Physiological Effects of the Cholinesterase Inhibitor Carbaryl (1-Naphthyl Methylcarbamate).. 1972. ...
Acetyl cholinesterase inhibitor. Neurotoxicant. No data found. XNo, known not to cause a problem ...
Case Studies in Environmental Medicine: Cholinesterase Inhibitors Including Pesticides and Chemical Warfare Nerve Agents. This ...
Rivastigmine is in a class of medications called cholinesterase inhibitors. It improves mental function (such as memory and ...
What is the role of acetyl cholinesterase inhibitors in the treatment of Alzheimer disease (AD) in Down syndrome (DS)? ... In addition, most studies of cholinesterase inhibitors were conducted in patients with mild-to-moderate disease, and efficacy ... Several studies in patients without DS suggest that both the cholinesterase inhibitors and memantine may effectively treat ... Donepezil remains the only cholinesterase inhibitor also approved to treat patients with severe dementia. ...
This long-acting cholinesterase inhibitor enhances the effect of endogenously liberated acetylcholine in iris, ciliary muscle, ... Long-acting, topical ophthalmic cholinesterase inhibitor that enhances effect of endogenously liberated acetylcholine in iris, ... Few weeks of therapy may depress plasma and erythrocyte cholinesterase levels. Perform baseline measurement of anterior chamber ... Echothiophate iodide ophthalmic solution will depress both plasma and erythrocyte cholinesterase levels in most patients after ...
These included cholinesterase inhibitors, N-methyl D-aspartate (NMDA) receptor antagonists, selective serotonin reuptake ... The researchers found Black patients who were referred to a neurologist received cholinesterase inhibitors and NMDA antagonists ... for cholinesterase inhibitors; 10% vs17% for NMDA-antagonists).. Black patients with dementia were also less likely to receive ...
Design, synthesis and biological evaluation of novel tricyclics as dual cholinesterase (ChE) and amyloid aggregation inhibitors ... Comparative risk of cardiac arrhythmias associated with acetylcholinesterase inhibitor use  Huang, Yichang (University of ...
Molecular design and synthesis of novel peptides from amphibians skin acting as inhibitors of cholinesterase enzymes ... Hydroxynaphthalenecarboxamides and substituted piperazinylpropandiols, two new series of BRAF inhibitors. A theoretical and ... Molecular Modeling Study of Dihydrofolate Reductase Inhibitors. Molecular Dynamics Simulations, Quantum Mechanical Calculations ... Synthesis and biological evaluation of sphingosine kinase 2 inhibitors with anti-inflammatory activity ...
The Mini-Mental State Examination (MMSE) also has been used in clinical trials of cholinesterase inhibitors, and although it is ... Monitoring the clinical effect of a cholinesterase inhibitor is difficult because of the varying symptoms and rate of decline ... There are no clinical trials directly assessing the best way to monitor patients on a cholinesterase inhibitor. The Alzheimers ... patients treated with cholinesterase inhibitors showed improvement by an average of 2.7 points.5 However, literature suggests ...
Note to Physicians and Veterinarians: This product contains tetrachlorvinphos which is a cholinesterase inhibitor. Cholinergic ... not use this product on animals simultaneously or within 30 days before or after treatment with or exposure to cholinesterase ...
Twenty-four topics are available, including chromium, cadmium, cholinesterase inhibitors, ethylene/propylene glycol, and ...
Cholinesterase inhibitors to increase levels of neurotransmitters to delay cognitive decline and memory loss ...
  • A Meeting on the topic "Latest Developments in Dementia - Alzheimer's Disease: From Cholinesterase Inhibitors to Stem Cell Treatment" was held at King George Hotel on February 22-23, 2008. (hygeia.gr)
  • Galantamine is used in the treatment of alzheimer's disease and belongs to the drug class cholinesterase inhibitors . (drugs.com)
  • How do you monitor patients with Alzheimer's disease to determine if they are benefiting from receiving a cholinesterase inhibitor? (aafp.org)
  • Of the many assessment tools validated for use in patients with Alzheimer's disease, there are several that demonstrate the effectiveness of cholinesterase inhibitors versus placebo in randomized controlled trials ( Table 1 11 , 12 ) . (aafp.org)
  • For Alzheimer's Disease associated memory loss cholinesterase inhibitors, such as tacrine (Cognex®), donepezil (Aricept®), rivastigmine (Exelon®) and galantamine (Reminyl®), have been beneficial. (clevelandclinicmeded.com)
  • Studies currently underway include evaluating the role of health specialists in treating depressed patients, looking at bereavement and its effects on patients, and the role of estrogen, vitamin E, NSAIDs and COX-2 inhibitors in preventing and treating Alzheimer's disease. (psychiatrictimes.com)
  • Cholinesterase inhibitors for Alzheimer's disease. (bvsalud.org)
  • Doses atropine for cholinesterase inhibitor toxicity (prescribed drugs, nerve gas, insecticides). (mdcalc.com)
  • Data are given for cholinesterase (9001085) levels of affected persons, symptoms, and details of dermatitis resulting from the insecticides and allergic reactions from celery juice and sunlight. (cdc.gov)
  • The treatment options for MG include medications such as acetylcholinesterase inhibitors, immunosuppressive drugs, and monoclonal antibodies that target the immune system. (marketresearchcommunity.com)
  • What laboratory tests are most helpful in guiding the emergency treatment of acute cholinesterase inhibitor toxicity? (cdc.gov)
  • What are the three major delayed adverse effects that can follow recovery from the acute cholinesterase toxicity? (cdc.gov)
  • Do not use this product on animals simultaneously or within 30 days before or after treatment with or exposure to cholinesterase inhibiting drugs, pesticides, or chemicals. (sergeants.com)
  • What are the major classifications of signs and symptoms characteristic of cholinesterase inhibitor poisoning? (cdc.gov)
  • Rivastigmine belongs to a family of medications known as cholinesterase inhibitors . (medbroadcast.com)
  • Rivastigmine is in a class of medications called cholinesterase inhibitors. (medlineplus.gov)
  • Patients are treated with medications, such as cholinesterase inhibitors, that are approved by the U.S. Food and Drug Administration for memory impairment. (psychiatrictimes.com)
  • Dichlorvos, an organophosphate, is a direct-acting cholinesterase (ChE)l inhibitor. (unep.org)
  • These included cholinesterase inhibitors, N -methyl D -aspartate (NMDA) receptor antagonists, selective serotonin reuptake inhibitors (SSRIs), antipsychotics, and benzodiazepines. (medscape.com)
  • The researchers found Black patients who were referred to a neurologist received cholinesterase inhibitors and NMDA antagonists at rates comparable to White patients. (medscape.com)
  • There are currently three cholinesterase inhibitors and one N-methyl-D-aspartate (NMDA) antagonist indicated in the treatment of AD as monotherapy or in combination. (bvsalud.org)
  • When cholinesterases are inhibited, the action of endogenously released acetylcholine at cholinergic synapses is potentiated. (bvsalud.org)
  • What are the major treatment strategies recommended in acute cholinesterase inhibitor poisoning? (cdc.gov)
  • What is the usual cause of death from acute cholinesterase inhibitor poisoning? (cdc.gov)
  • Acute and chronic effects of cholinesterase inhibitors and pilocarpine on the density and sensitivity of central and peripheral alpha 2-adrenoceptors. (bvsalud.org)
  • Acute (12 h), short-term (4 days) or chronic (7-18 days) treatment with the cholinesterase inhibitors neostigmine (0.1 mg/kg), physostigmine (0.1 mg/kg) and diisopropylfluorophosphate (2 mg/kg) and with the muscarinic receptor agonist pilocarpine (10 mg/kg) did not alter the density of brain alpha 2- adrenoceptors . (bvsalud.org)
  • What aspects of this situation suggest toxic exposure to a cholinesterase inhibitor? (cdc.gov)
  • Recommendations include monitoring of pre- exposure cholinesterase levels, checking of red blood cell or plasma decrease, provision of protective equipment and facilities for maintaining good personal hygiene, and informing farm ers of safety measures. (cdc.gov)
  • What is the pathophysiology underlying the clinical findings in cholinesterase inhibitor poisoning? (cdc.gov)
  • The clinical findings of eye pain, blurred or dim vision, respiratory distress, diaphoresis and seizures are all consistent with cholinesterase inhibitor poisoning. (cdc.gov)
  • There are no clinical trials directly assessing the best way to monitor patients on a cholinesterase inhibitor. (aafp.org)
  • The Mini-Mental State Examination (MMSE) also has been used in clinical trials of cholinesterase inhibitors, and although it is familiar to most physicians, it lacks specificity. (aafp.org)
  • Cholinesterase inhibitors remain the first-line therapy in patients with mild to moderate AD, which may stabilise the symptomatic cognitive and functional decline. (bvsalud.org)
  • 2 , 4 Over the first six to 12 months, patients treated with cholinesterase inhibitors showed improvement by an average of 2.7 points. (aafp.org)
  • Behavioral and Physiological Effects of the Cholinesterase Inhibitor Carbaryl (1-Naphthyl Methylcarbamate). (epa.gov)
  • Other pharmacotherapy options include the use of memantine which may be used by itself or in combination with cholinesterase inhibitors. (bvsalud.org)
  • Since the introduction of the first cholinesterase inhibitor (ChEI) in 1997, most clinicians and probably most patients would consider the cholinergic drugs, donepezil, galantamine and rivastigmine, to be the first line pharmacotherapy for mild to moderate Alzheimer's disease.The drugs have slightly different pharmacological properties, but they all work by inhibiting the breakdown of acetylcholine, an important neurotransmitter associated with memory, by blocking the enzyme acetylcholinesterase. (nih.gov)
  • All 4 currently approved ChEIs (ie, donepezil, rivastigmine, galantamine) inhibit acetylcholinesterase (AChE) at the synapse (specific cholinesterase). (medscape.com)
  • Rivastigmine is a potent, selective inhibitor of brain AChE and BChE. (medscape.com)
  • Rivastigmine is considered a pseudo-irreversible inhibitor of AChE. (medscape.com)
  • The cholinesterase inhibitors (ChEIs) donepezil and rivastigmine are used to ease the symptoms of dementia associated with AD. (nih.gov)
  • Galantamine, rivastigmine, and donepezil are cholinesterase inhibitors that are prescribed for mild to moderate Alzheimer's symptoms. (nih.gov)
  • Rivastigmine is in a class of medications called cholinesterase inhibitors. (medlineplus.gov)
  • Donepezil transdermal is a reversible acetylcholinesterase inhibitor. (medscape.com)
  • Cholinesterase inhibitors (ChEIs) are used to palliate cholinergic deficiency. (medscape.com)
  • Because cholinesterase inhibitors work in a similar way, switching from one to another may not produce significantly different results, but a person living with Alzheimer's may respond better to one drug versus another. (nih.gov)
  • The mainstay of therapy for patients with Alzheimer disease (AD) is the use of centrally acting cholinesterase inhibitors to attempt to compensate for the depletion of acetylcholine (ACh) in the cerebral cortex and hippocampus. (medscape.com)
  • This is accomplished by increasing the concentration of acetylcholine through reversible inhibition of its hydrolysis by cholinesterase. (medscape.com)
  • Cholinesterase inhibitors prevent the breakdown of acetylcholine, a brain chemical believed to be important for memory and thinking . (nih.gov)
  • The clinical findings of eye pain, blurred or dim vision, respiratory distress, diaphoresis and seizures are all consistent with cholinesterase inhibitor poisoning. (cdc.gov)
  • What are the three major delayed adverse effects that can follow recovery from the acute cholinesterase toxicity? (cdc.gov)