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As a result of cholinergic crisis, the muscles stop responding to the high synaptic levels of acetylcholine, leading to flaccid paralysis, respiratory failure, and other signs and symptoms reminiscent of organophosphate poisoning. Other symptoms include increased sweating, salivation, bronchial secretions along with miosis (constricted pupils).
Chemical structure of acetylcholine. Cholinergic blocking drugs are a group of drugs that block the action of acetylcholine (ACh), a neurotransmitter, in synapses of the cholinergic nervous system. [1] They block acetylcholine from binding to cholinergic receptors, namely the nicotinic and muscarinic receptors.
Individuals symptoms vary in severity and type. Severe, subacute gastrointestinal dysmotility and orthostatic hypotension are the most common symptoms in two-thirds of patients. Symptoms can be severe in some cases and gradually worsen in others. [1] Sympathetic failure manifests itself as orthostatic hypotension and anhidrosis.
At high glucose levels, glycolysis takes place rapidly, thus increasing the amount of citrate produced from the citric acid cycle. This citrate is then exported to other organelles outside the mitochondria to be broken into acetyl-CoA and oxaloacetate by the enzyme ATP citrate lyase (ACL). This principal reaction is coupled with the hydrolysis ...
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The resulting decrease in acetylcholine in the brain is thought to contribute to the decline in mental function of affected patients. [ 3 ] [ 2 ] For this reason, most currently available pharmacological treatments for dementia focus on compensating for faltering function of the nucleus basalis through artificially increasing acetylcholine levels.
Acetylcholinesterase (HGNC symbol ACHE; EC 3.1.1.7; systematic name acetylcholine acetylhydrolase), also known as AChE, AChase or acetylhydrolase, is the primary cholinesterase in the body. It is an enzyme that catalyzes the breakdown of acetylcholine and some other choline esters that function as neurotransmitters :