Studies have confirmed that the thalamus and the primary somatosensory cortex (SI) are associated with cognitive function. These two brain regions are closely related in structure and function. The interactions between SI and the thalamus are of crucial significance for the cognitive process. Patients with major depressive disorder (MDD) have significant cognitive impairment. Based on these observations, we used resting-state functional magnetic resonance imaging (rs-fMRI) to investigate whether there is an abnormality in the SI-thalamic functional connection in MDD. Furthermore, we explored the clinical symptoms related to this abnormality. We included 31 patients with first-episode major depressive disorder and 28 age-, gender-, and education-matched healthy controls (HC). The SI-thalamic functional connectivity was compared between the MDD and HC groups. The correlation analyses were performed between areas with abnormal connectivity and clinical characteristics. Compared with healthy subjects, the MDD patients had enhanced functional connectivity between the thalamus and SI (p < 0.05, corrected). Brain areas with significantly different levels of connectivity had a negative correlation with the Assessment of Neuropsychological Status total score (r = − 0.383, p = 0.033), delayed memory score (r = − 0.376, p = 0.037) and two-digit continuous operation test score (r = − 0.369, p = 0.041) in MDD patients. These results demonstrate that SI-thalamic functional connectivity is abnormal and associated with the core clinical symptoms in MDD. The SI-thalamic functional connectivity functions as a neurobiological feature and potential biomarker for MDD.

Major depressive disorder (MDD) is a significant contributor to global disease burden, with somatic symptoms frequently complicating its diagnosis and treatment. Recent advances in neuroimaging have provided insights into the neurobiological underpinnings of MDD, yet the role of the glymphatic system remains largely unexplored. This study aimed to assess glymphatic function in drug-naïve somatic depression (SMD) patients using the diffusion tensor image analysis along the perivascular space (DTI-ALPS) index. A total of 272 participants, including somatic depression patients (SMD), pure depression (PMD), and healthy controls (HC), were enrolled. We collected T1-weighted (T1w) and DTI (diffusion tensor image) scans and clinical data of all participants. The DTI-ALPS indices were calculated and compared among three groups. Gray matter regions associated with the DTI-ALPS index were identified by voxel-based morphometry analysis (VBM), revealing a cluster located in the thalamus. Then, we performed partial correlation analyses to further investigate the relationships between the DTI-ALPS index, thalamic volume, and clinical data. The DTI-ALPS index was significantly higher in the MDD group compared to the HC group, particularly in the SMD group. Furthermore, a significant positive correlation was observed between the DTI-ALPS index and thalamic volume, with lower DTI-ALPS values associated with reduced thalamic volumes, especially in the SMD group. Our findings suggest heightened glymphatic activity in MDD patients, especially SMD patients, and a potential link between glymphatic function and thalamic vulnerability. Therefore, the thalamus' vulnerability to glymphatic system function may play a role in the pathophysiology of depression, particularly somatic depression, suggesting that both the glymphatic system and the thalamus could serve as potential therapeutic or intervention targets for future treatments.

Background: Cortical morphometry is an intermediate phenotype that is closely related to the genetics and onset of major depressive disorder (MDD), and cortical morphometric networks are considered more relevant to disease mechanisms than brain regions. We sought to investigate changes in cortical morphometric networks in MDD and their relationship with genetic risk in healthy controls. Methods: We recruited healthy controls and patients with MDD of Han Chinese descent. Participants underwent DNA extraction and magnetic resonance imaging, including T₁-weighted and diffusion tensor imaging. We calculated polygenic risk scores (PRS) based on previous summary statistics from a genome-wide association study of the Chinese Han population. We used a novel method based on Kullback–Leibler divergence to construct the morphometric inverse divergence (MIND) network, and we included the classic morphometric similarity network (MSN) as a complementary approach. Considering the relationship between cortical and white matter networks, we also constructed a streamlined density network. We conducted group comparison and PRS correlation analyses at both the regional and network level. Results: We included 130 healthy controls and 195 patients with MDD. The results indicated enhanced connectivity in the MIND network among patients with MDD and people with high genetic risk, particularly in the somatomotor (SMN) and default mode networks (DMN). We did not observe significant findings in the MSN. The white matter network showed disruption among people with high genetic risk, also primarily in the SMN and DMN. The MIND network outperformed the MSN network in distinguishing MDD status. Limitations: Our study was cross-sectional and could not explore the causal relationships between cortical morphological changes, white matter connectivity, and disease states. Some patients had received antidepressant treatment, which may have influenced brain morphology and white matter network structure. Conclusion: The genetic mechanisms of depression may be related to white matter disintegration, which could also be associated with decoupling of the SMN and DMN. These findings provide new insights into the genetic mechanisms and potential biomarkers of MDD.

Background: There is a high correlation between the risk of major depressive disorder (MDD) and adverse childhood experiences (ACEs) such as adverse parenting (AP). While there appears to be an association between ACEs and changes in brain structure and function, there have yet to be multimodal neuroimaging studies of associations between parenting style and brain developmental changes in MDD patients. To explore the effect of AP on brain structure and function. Methods: In this cross-sectional study, 125 MDD outpatients were included in the study and divided into the AP group and the optimal parenting (OP) group. Participants completed self-rating scales to assess depressive severity, symptoms, and their parents’ styles. They also completed magnetic resonance imaging within one week of filling out the instruments. The differences between groups of gender, educational level, and medications were analyzed using the chi-squared test and those of age, duration of illness, and scores on scales using the independent samples t-test. Differences in gray matter volume (GMV) and resting-state functional connectivity (RS-FC) were assessed between groups. Results: AP was associated with a significant increase in GMV in the right superior parietal lobule (SPL) and FC between the right SPL and the bilateral medial superior frontal cortex in MDD patients. Limitations: The cross-cultural characteristics of AP will result in the lack of generalizability of the findings. Conclusions: The results support the hypothesis that AP during childhood may imprint the brain and affect depressive symptoms in adulthood. Parents should pay attention to the parenting style and avoid a style that lacks warmth.