Dopamine dysfunction beyond psychosis: Reevaluating its role in depression, anxiety, and obsessive-compulsive disorder.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic and clinical literature without systematic review methodology
PubMed 41564196 · doi:10.24869/psyd.2025.295
What was done
This review synthesized literature evaluating dopamine dysregulation as a transdiagnostic mechanism across major depressive disorder, anxiety disorders, and obsessive-compulsive disorder (OCD). It examined implicated neural circuits (mesolimbic, mesocortical, and cortico-striatal-thalamo-cortical loops), shared symptom dimensions, etiological factors including inflammation and gene-environment interactions, and potential dopaminergic pharmacological and neuromodulatory treatments.
What was found
The abstract reports no quantitative values or statistical effect sizes. It qualitatively describes consistent patterns of dopamine dysregulation across mesolimbic, mesocortical, and cortico-striatal-thalamo-cortical circuits linked to symptom domains like anhedonia, apathy, compulsivity, and cognitive inflexibility. It notes that dopaminergic agents (e.g., bupropion, pramipexole, aripiprazole) and neuromodulation (e.g., TMS, DBS) show promise, particularly in treatment-resistant or subtype-specific presentations.
Why it matters
The review organizes evidence positioning dopaminergic deficits as a transdiagnostic mechanism beyond psychosis, supporting biomarker-guided and circuit-based approaches for depression, anxiety, and OCD.
Limits
As a narrative review, the abstract provides no systematic search strategy, selection criteria, risk-of-bias assessment, or quantitative meta-analysis. No sample sizes or study-level counts are reported, and the claims rely on synthesized secondary literature and mechanistic models rather than original empirical data.
Cited by
- supports Obsessive-compulsive disorder is directly tied to the brain's dopamine pathway.