Shared and disease-sensitive dysfunction across bipolar and unipolar disorder during depressive episodes: a transdiagnostic study.

Patients with depressive episodes (PDE), such as unipolar disorder (UD) and bipolar disorder (BD), are often defined as distinct diagnostic categories, but increasing converging evidence indicated shared etiologies and pathophysiological characteristics across different clinical diagnoses. We explored whether these transdiagnostic deficits are caused by the common neural substrates across diseases or disease-sensitive mechanisms, or a combination of both. In this study, we utilized a Bayesian model to decompose the resting-state brain activity into multiple hyper- and hypo-activity patterns (refer to as "factors"), so as to explore the shared and disease-sensitive alteration patterns in PDE. The model was constructed over a total of 259 patients (131 UD and 128 BD) with 100 healthy controls as the reference. The other 32 initial depressive episode BD (IDE-BD) patients who had symptoms of mania or hypomania during follow-up were taken as an independent set to estimate the factor composition using the established model for further analysis. We revealed three transdiagnostic alteration factors in PDE. Based on the distribution of factors and the tendency of factor composition at the group level, these factors were defined as BD sensitive factor, UD sensitive factor and shared basic alteration factor. We further found that the factor composition and the ROIs-based alteration degree (mainly involving in orbitofrontal gyrus and part of parietal lobe) were associated with the bipolar index in IDE-BD patients. Our findings contributed to understanding the core transdiagnostic shared and disease-sensitive alterations in PDE and to predicting the risk of emotional state transition in IDE-BD patients.