Acetylcholinesterase

Nerve cells that use acetylcholine release it into the synaptic cleft, the narrow gap between one cell and the next. AChE removes acetylcholine from that gap after the electrical signal has been passed on, which makes the enzyme an essential part of chemical signaling between nerve cells [1]. In this way it ends each signal at cholinergic synapses, the junctions that run on acetylcholine [2].

The enzyme's shape helps explain its speed [2]. Its active site sits at the bottom of a deep, narrow gorge in the protein, a layout researchers did not expect given how fast the enzyme works [2]. More than 300 structures of AChE have been published, including some bound to drugs [1].

AChE is a major target for medicines used in a variety of neurological conditions [1]. It is also the target of organophosphorus compounds, used as pesticides and chemical warfare agents, which bind to the enzyme's active site [1].

A supplement paper may report that an extract inhibited AChE, meaning it slowed the enzyme down. Because AChE is what clears acetylcholine from the synapse [1], slowing it is one proposed way a compound could act on acetylcholine signaling. That makes AChE inhibition a mechanism.

A mechanism result is not an effect on thinking. A test-tube assay, or a lower AChE reading in a blood sample, does not show that memory or attention changed. A trial might report AChE activity and memory scores side by side, and the two results are read separately. On NootropicsWork, enzyme findings are labeled as mechanism, and grades are given only for outcomes measured in people, such as memory, attention or mood.

Watch the name, too. Acetylcholine is the messenger, and acetylcholinesterase is the enzyme that breaks it down [1].

• Choline: one of the two products when AChE breaks down acetylcholine.
• Acetylcholine: the messenger AChE clears.