Acetylcholinesterase inhibitor

[4][5] Organophosphates like tetraethyl pyrophosphate (TEPP) and sarin inhibit cholinesterases, enzymes that hydrolyze the neurotransmitter acetylcholine.

Important amino acid residues in the esteratic site are a glutamate, a histidine, and a serine.

[citation needed] At the esteratic site the acetylcholine is cleaved, which results in a free choline moiety and an acetylated cholinesterase.

This phosphorylation inhibits the binding of the acetyl group of the acetylcholine to the esteratic site of the cholinesterase.

This results in continuous activation of acetylcholine receptors, which leads to the acute symptoms of TEPP poisoning.

[6] In this formula, E is the remaining enzyme activity, E0 is the initial enzyme activity, t is the time interval after mixing of the cholinesterase and the TEPP, KI is the dissociation constant for cholinesterase-TEPP complex (E–PX) and I is the TEPP concentration.

It is believed that the neuropathy target esterase (NTE) is affected by the organophosphate which induces the disease.

These guidelines, known as the Medication Appropriateness Tool for Comorbid Health conditions in Dementia (MATCH-D), suggest that these medicines are at least considered.

[4] When used in the central nervous system to alleviate neurological symptoms, such as rivastigmine in Alzheimer's disease, all cholinesterase inhibitors require doses to be increased gradually over several weeks, and this is usually referred to as the titration phase.

This strategy is used to build tolerance to adverse events or to reach a desired clinical effect.

These include: Compounds which function as quasi-irreversible inhibitors of cholinesterase are those most likely to have use as chemical weapons or pesticides.