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It is an enzyme that catalyzes the breakdown of acetylcholine and some other choline esters that function as neurotransmitters: acetylcholine + H 2 O = choline + acetate. It is found at mainly neuromuscular junctions and in chemical synapses of the cholinergic type, where its activity serves to terminate cholinergic synaptic transmission.
A cholinergic crisis is an over-stimulation at a neuromuscular junction due to an excess of acetylcholine, [1] as a result of the inactivity of the acetylcholinesterase enzyme, which normally breaks down acetylcholine.
Acetylcholine Acetylcholinesterase Acetylcholinesterase inhibition. Acetylcholinesterase inhibitors (AChEIs) also often called cholinesterase inhibitors, [1] inhibit the enzyme acetylcholinesterase from breaking down the neurotransmitter acetylcholine into choline and acetate, [2] thereby increasing both the level and duration of action of acetylcholine in the central nervous system, autonomic ...
The enzyme acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle ...
These drugs work to increase the levels of acetylcholine and subsequently increase the function of neural cells. [8] However, not all treatments based upon the cholinergic hypothesis have been successful in treating the symptoms or slowing the progression of AD. [9]
Acetylcholine (ACh) is an organic compound that functions in the brain and body of many types of animals (including humans) as a neurotransmitter. [1] Its name is derived from its chemical structure: it is an ester of acetic acid and choline. [2] Parts in the body that use or are affected by acetylcholine are referred to as cholinergic.
Cholinesterase inhibitors (ChEIs), also known as anti-cholinesterase, are chemicals that prevent the breakdown of the neurotransmitter acetylcholine or butyrylcholine by cholinesterase. This increases the amount of the acetylcholine or butyrylcholine in the synaptic cleft that can bind to muscarinic receptors, nicotinic receptors and others.
The mechanism currently known that operates via the synaptic cleft causing impairment of normal functioning is another congenital myasthenia gravis.(reference 7) This mechanism is the only currently known disease that acts on the synapse.(reference 12) It acts by impairing the function of the enzyme that breaks down acetylcholine causing it to ...