# Dopamine Hypothesis of Schizophrenia

Dopamine dysregulation is relevant to psychosis and symptom modulation; unselected mesolimbic D2 primacy is not established.

Overall Γ follows registered SC3, with association SC1 at Β and a conservative Γ for the strictly audited SC2 mechanism gate. The nominal claim fixes mesolimbic anatomy and unselected primacy, whereas strong human findings often concern associative striatum or symptom-responsive contexts. Clinical symptom modulation remains supported; the unresolved exact causal-primacy claim cannot be rescued by changing the anatomical label or retrospectively selecting responders.

Treatment status, positive-symptom state, compartment and resistant-versus-responsive comparisons map boundaries. Group differences do not prospectively validate a response-selected human causal subtype. No post-hoc restriction replaces registered unselected SC3.