Monoamine hypothesis of depression

A family of proposals relating depression to reduced or dysregulated monoamine signalling. A simple universal deficiency account is stronger than the claim that a monoaminergic manipulation can alter symptoms. Drug-target engagement, therapeutic mediation and original disease cause are separate causal claims.

An experimental manipulation intended to reduce the availability of the serotonin precursor tryptophan. Effects in a previously treated remitted sample test dependence of that state on precursor availability; they do not directly measure a universal baseline serotonin deficit.