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Tian-Mei Si

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Aug 2026

The Inter-Relationships of Depressive and Anxiety Symptoms with Suicidality Among Asian Psychiatric Patients: Findings From the REAP-AD3.

BACKGROUND Depressive and anxiety symptoms (depression and anxiety hereafter), and suicidality are common among psychiatric patients. This study examined the network structure of depressive and anxiety symptoms and suicidality among psychiatric patients across Asia. METHODS Data were drawn from the Research on Asian Psychotropic Prescription Patterns for Antidepressants Phase 3 study (REAP-AD3), which included 2,455 psychiatric patients from 11 Asian countries and territories. Depression and anxiety were assessed using the 9-item Patient Health Questionnaire (PHQ-9) and 7-item Generalized Anxiety Disorder Scale (GAD-7), respectively, while suicidality (i.e., suicidal thoughts or acts) was assessed by a clinical interview. Expected Influence (EI) and Bridge EI were used as centrality indices in the symptom network to characterize the structure of the symptoms. RESULTS The point prevalence of suicidality was 30.1% (95% confidence interval [CI] = 28.2, 31.9) among the psychiatric patients. The network analysis identified PHQ2 ("Sad mood") as the most central symptom, followed by GAD2 ("Uncontrollable worry"). Additionally, PHQ8 ("Motor disturbances") and S ("Suicidality") were identified as bridge nodes linking depression and anxiety with suicidality. The flow network indicated that PHQ6 ("Guilt") and PHQ2 ("Sad mood") had the strongest positive associations with suicidality. CONCLUSIONS Suicidality was common among psychiatric patients across Asia. The central and bridge symptoms might represent potential clinical markers and generate hypotheses for longitudinal and interventional research on depression, anxiety, and suicidality in the future.

L. A, Yuan Feng, Qinge Zhang et al. · International Journal of Soc... · 0 citations

Review Open access Jul 2026

Mitochondrial-inflammation crosstalk in major depressive disorder: molecular mechanisms and therapeutic implications.

Despite its high prevalence, the precise mechanisms underlying major depressive disorder (MDD) remain incompletely understood. Growing evidence identifies mitochondrial dysfunction, including abnormalities in mitochondrial DNA, impaired bioenergetics, disrupted quality control, and redox imbalance, as a central pathological feature of MDD. Beyond deficits in energy production, mitochondria function as upstream regulators of neuroinflammation. Mitochondria derived damage associated molecular patterns and excessive reactive oxygen species activate innate immune signaling, while inflammatory challenges in turn compromise mitochondrial integrity. This bidirectional and self-reinforcing interaction between mitochondrial dysfunction and inflammation may contribute to disease onset, progression, and clinical heterogeneity. Preclinical and clinical studies indicate that conventional antidepressants gradually restore mitochondrial function while suppressing oxidative and inflammatory stress, whereas rapid-acting agents such as ketamine induce acute metabolic reprogramming and mitophagy, enabling swift functional recovery. Mechanistically distinct interventions, including mitochondria targeted antioxidants, metabolic modulators, and psychedelic compounds, further highlight the therapeutic potential of targeting mitochondrial pathways. By integrating current evidence, this review delineates mitochondrial-inflammation crosstalk in MDD and supports mitochondrial regulation as a promising target for novel antidepressant strategies.

Yu Wang, Ji‐Tao Li, Lin-lin Zhu et al. · Molecular Psychiatry · 1 citation