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The age of onset (AOO) is a key factor for heterogeneity in major depressive disorder (MDD). Looking at the effect of AOO on symptomatology may improve clinical outcomes. This study aims to examine whether and how AOO affects symptomatology using a machine learning approach and latent profile analysis (LPA).The study enrolled 915 participants diagnosed with MDD from eight hospitals across China. Depressive symptoms were assessed using the 17-item Hamilton Depression Rating Scale. The relationship between symptom profiles and AOO was explored using Random Forest. The effect of AOO on symptom clusters and subtypes was investigated using multiple linear regression and LPA. A continuous AOO indicator was used to conduct the analyses.Based on the Random Forest, symptom profiles were closely associated with AOO. The regression model showed that the severity of neurovegetative symptoms was positively associated with AOO (β = 0.18, p 0.001), and the severity of cognitive-behavioral symptoms was negatively associated with AOO (β = -0.12, p 0.001). LPA demonstrated that the subgroups characterized by suicide and guilt had earlier onset of depression. The subgroup with the lowest global severity of depression had the latest onset.AOO was recalled retrospectively. The relative scarcity of participants with childhood and adolescence onset depression.AOO has an important impact on symptomatology. The findings may enhance clinical evaluations for MDD and assist clinicians in promoting earlier detection and individualized care in vulnerable individuals.

Background This study aimed to explore subtypes of treatment-resistant depression (TRD). Methods Latent class analysis (LCA) was performed on clinical and demographic data collected from 375 patients with TRD. Clinical variables were compared across subtypes. Treatment outcomes across subtypes of TRD were compared separately for those within each subtype with anxiety (those with a HRSD-17 anxiety/somatization factor score ≥ 7) and those without anxiety. LCA subtypes were compared using Cochran's and Mantel–Haenszel χ2 test, respectively. Unordered multinomial logistic regression was used to assess clinical correlates of TRD subtypes. Results Three categories were detected: severe depression (66%), moderate depression with anxiety (9%) and mild depression with anxiety/somatization (25%). Gender, age, age at first onset, family monthly income, number of hospitalizations, HRSD-17 and clinical global impression-severity (CGI) scores were significantly different across the three groups. Remission rates were significantly different among anxious cases with severe (43.75%), moderate (22.73%) and mild (26.25%) depression subtypes. Compared to cases in the mild depression group, those in the severe depression group had a greater likelihood of being male, having a later age of first onset, higher numbers of hospitalization, higher HRSD-17 and CGI total scores, and lower family income. Those in the moderate depression group were more likely to be male and have lower family income than those in the mild depression group. Limitations Representative bias, relatively small sample size, unbalanced group size and incomplete indicator variables might have a negative effect on the validity and generalization of the findings. Conclusions Depression severity could be a basis for subtype classification of patients with TRD. The classification of latent class of TRD observed in our study was similar to the structure found in MDD. Longitudinal research into the stability of the latent structure of TRD across illness course is merited as is research into treatment outcomes for TRD subtypes.

Somatic symptoms are prevalent in patients with major depressive disorder (MDD) and often associated with a high risk of suicide. However, which somatic symptoms display as significant risk factors for suicidal ideation (SI) is still poorly understood in MDD.Two thousand and seventeen Chinese patients with first-episode MDD from the National Survey on Symptomatology of Depression were included in this study. A doctor-rating assessment questionnaire was constructed to evaluate depression related somatic symptoms, and stepwise logistic regression analysis was performed to explore the relationship between somatic symptoms and SI.Our results showed a high prevalence of current SI in first-episode MDD (50.87%), while no significant gender differences (53.32% vs. 49.26%, P = 0.076) were observed. In addition, patients who have more somatic symptoms would be at the higher risk to elicit SI, and stepwise logistic regression analysis indicated that age (β = -0.020, P 0.001), Pre-verbal physical complaints (β = 0.356, P = 0.001), Sensory system complaints (β = 0.707, P = 0.000), Other pain conditions (β = 0.434, P 0.001), Late insomnia (β = 0.267, P = 0.008), Hypersomnia (β = 0.936, P 0.001), Weight loss (β = 0.272, P = 0.006), Hyposexuality (β = 0.513, P = P 0.001) were strongly associated with current SI in first-episode Chinese major depression.Somatic symptoms are strongly associated with SI in first-episode MDD. It is suggestive for clinicians to show concerns for patients' somatic symptoms in practice.

It has been suggested that inflammation is involved in the pathophysiology of depression. As tissue-specific macrophages in the central nervous system (CNS), microglia play an important role in neuroinflammation. Resident microglia become activated towards the pro-inflammatory (M1) phenotype or the anti-inflammatory (M2) phenotype during neuroinflammation. In the CNS, neurons report to microglia regarding their statuses and can regulate microglial activation, while microglia also modulate neuronal activities, including neuroplasticity. The molecular mechanisms underlying the communication between microglia and neurons, which include intracellular and extracellular signalling pathways, might be complex and of great importance for new research on the pathogenesis of depression. The present review aims to discuss the common cellular and molecular mechanisms for microglial activation and aberrant neuroplasticity in depression and the role of these processes in the pathogenesis of depression.