acetylcholinesterase

An acetylcholinesterase inhibitor such as the Donepezil used in the article inhibits the action of acetylcholinesterase, which in turn enhances acetylcholine neurotransmission in a dose-dependent manner.

Odysseus prevented succumbing to Circe's poison by taking galantamine from the flowers of Galanthus nivalis, which is an acetylcholinesterase inhibitor.

Briefly: Acetylcholinesterase terminates acetylcholine neurotransmission events by deactivating the acetylcholine, allowing it to be reused.

Downside: increased blood pressure and sustained high levels of heart rate, adesonine reuptake inhibitor and mildly addictive through dopaminegic pathways, acetylcholinesterase inhibitor.

They mention Modafinil (an atypical stimulant), Donepezil (an acetylcholinesterase inhibitor) and beta blockers.

Arricept, Huperzine, and other chemicals inhibit acetylcholinesterase formation (and therefore increase acetylcholine levels).

Out of curiosity, what simpler term would you instead use for 'acetylcholinesterase inhibitor'?

This compound is an acetylcholinesterase inhibitor, so it increases acetylcholine in the brian.

It could also be that the microplastics can physically bind to or chemically inhibit acetylcholinesterase and that is the reason for the higher acetylcholine.

Lately, I've been just taking Huperzine A, which acts as an acetylcholinesterase inhibitor.

Highly potent acetylcholinesterase inhibitors are used as poisons (Sarin gas, for example) because they interfere with all of the acetylcholine-based neurotransmission that happens throughout your brain and body.

Reelin is transcribed 4 genes away from acetylcholinesterase.

The very next sentence continues: "Additionally, exposure to micro- and nanoplastics can result in inhibition of acetylcholinesterase activity and altered neurotransmitter levels, which both may contribute to the reported behavioral changes." (emphasis again mine).

If you live in a developed country where people aren't repeatedly killing themselves through acute exposure the relevant section of the link above appears to be: "The US EPA concluded in 2016 that the existing epidemiologic literature provided “sufficient evidence that there are neurodevelopmental effects occurring at chlorpyrifos exposure levels below that required to cause acetylcholinesterase inhibition” [11].

Acetylcholinesterase inhibitors are a very blunt and non-specific way to manipulate that neurotransmission.