first of all, cholinesterase is an enzyme not a hormone.
Now, about its overproduction: I don’t really think it would make that much of a difference. The fact this(i think), there is already enough cholinesterase in the synaptic cleft to quickly degrade any molecules of acetylcholine that are not attached to the receptor. In an extreme cases, the cholinesterase would simply block the nerve impulse, having similar effects to those of specific inhibitors of the nicotinic and muscarinic acetylcholine receptors.