Search

Abstract Background Childhood maltreatment (CM) is linked to long-term adverse health outcomes, including accelerated biological aging and cognitive decline. This study investigates the relationship between CM and various aging biomarkers: telomere length, facial aging, intrinsic epigenetic age acceleration (IEAA), GrimAge, HannumAge, PhenoAge, frailty index, and cognitive performance. Methods We conducted a Mendelian randomization (MR) study using published GWAS summary statistics. Aging biomarkers included telomere length (qPCR), facial aging (subjective evaluation), and epigenetic age markers (HannumAge, IEAA, GrimAge, PhenoAge). The frailty index was calculated from clinical assessments, and cognitive performance was evaluated with standardized tests. Analyses included Inverse-Variance Weighted (IVW), MR Egger, and Weighted Median (WM) methods, adjusted for multiple comparisons. Results CM was significantly associated with shorter telomere length (IVW: β = − 0.1, 95% CI − 0.18 to − 0.02, pFDR = 0.032) and increased HannumAge (IVW: β = 1.33, 95% CI 0.36 to 2.3, pFDR = 0.028), GrimAge (IVW: β = 1.19, 95% CI 0.19 to 2.2, pFDR = 0.040), and PhenoAge (IVW: β = 1.4, 95% CI 0.12 to 2.68, pFDR = 0.053). A significant association was also found with the frailty index (IVW: β = 0.31, 95% CI 0.13 to 0.49, pFDR = 0.006). No significant associations were found with facial aging, IEAA, or cognitive performance. Conclusions CM is linked to accelerated biological aging, shown by shorter telomere length and increased epigenetic aging markers. CM was also associated with increased frailty, highlighting the need for early interventions to mitigate long-term effects. Further research should explore mechanisms and prevention strategies.

Abstract Background For adolescents with major depression who exhibit suicidal tendencies, Electroconvulsive Therapy (ECT) is increasingly adopted in clinical practice. Yet, the precise mechanisms behind its effectiveness remain elusive, and studies on factors that influence treatment outcomes are scarce. Methods In this retrospective comparative study, we included all adolescent severe depressive episode patients with suicidal tendencies admitted to the Psychiatry Department of the First Affiliated Hospital of Chongqing Medical University between 2017 and 2021 and received ECT treatment. By collecting data on personal history, medical history, and standard treatment features, we established demographic, disease, medication, and ECT treatment factors variables. Patients were divided into effective and ineffective groups based on the Clinical Global Impressions-Improvement (CGI-I) scale scores, and differences between outcomes were compared. Logistic regression analyses were used to identify factors independently associated with ineffectiveness. Results A total of 494 adolescent severe depressive episode patients with suicidal behavior who received ECT were included in this study. According to CGI-I scores, the treatment was effective in 361 patients (73.1%) and ineffective in 133 patients (26.9%). Logistic regression analyses showed that 8 to 12 and 12 to 16 ECT sessions reduced the risk of ineffectiveness compared to fewer than 4 sessions. The risk of ineffectiveness decreased with age and increased with comorbidity with obsessive–compulsive disorder (OCD). Compared to sertraline, escitalopram was associated with a heightened risk of futility, whereas olanzapine and aripiprazole demonstrated a reduced risk when contrasted with quetiapine. Conclusions ECT's ineffectiveness in treating adolescent severe depressive episode with suicidal behavior decreases with age, and comorbidity with OCD significantly increases the risk of treatment failure. Fewer than 8 ECT sessions may hinder achieving satisfactory results.

Abstract Background Subacute combined degeneration of the spinal cord (SCD) is mainly caused by deficiency of Vitamin B12 and characterized by deep hypoesthesia, sensory ataxia and spasmodic paralysis of lower limbs. SCD often accompanies with megaloblastic anemia. Psychiatric symptoms could be the initial manifestations of SCD by lack of Vitamin B12, but are rarely considered secondary to physical discomfort and psychological factors in SCD. Additionally, treatment experience for psychiatric symptoms in SCD remains little reported. Case report We presented a case of a 37-year-old female who complained of being persecuted and controlled for one week and thus was admitted to the psychiatry department. Before that, she had went through persistent paresthesia and numbness of her lower extremities for two-month. Low Vitamin B12 level and hemoglobin concentration, neurologic symptoms and bone marrow smear results supported the clinical diagnosis of SCD and megaloblastic anemia. With supplementation of Vitamin B12 and blood transfusion and short-term prescription of antipsychotics and antidepressants, physical symptoms were improved and psychological symptoms disappeared within 2 weeks. Conclusions Psychiatric symptoms of SCD could be generated from lack of Vitamin B12, anemia and neurologic symptoms, where short-term use of antipsychotics and antidepressants may be effective.

Background: This study aims to investigate the association between nine tag single nucleotide polymorphisms (SNPs) in the C3 gene locus and the risk of coronary artery disease (CAD) as well as lipid levels in the Chinese population, and to further explore the interactions between SNPs and environmental factors that may be associated with CAD risk. Methods: A case-control study was conducted to investigate the association between CAD and C3 gene polymorphisms in a hospital setting. The study consisted of 944 CAD patients with a mean age of 55.97 ± 10.182 years and 897 non-CAD controls with a mean age of 55.94 ± 9.162 years. There were 565 males and 288 females in the CAD group and 583 males and 314 females in the control group. TagSNPs in the C3 gene were identified by employing the improved multiplex ligation detection reaction (iMLDR) technique, and multifactor dimensionality reduction (MDR) analysis was utilized to investigate the C3 gene–environment and gene–gene interactions in relation to the risk of CAD. Results: Results of the polymorphism study indicated that the CC genotype of rs7257062 was more frequent in the CAD group compared to the control group (10.9% vs 7.7%), with a statistically significant difference (p = 0.009). Moreover, the TT and CC + CT genotype groups of rs7257062 in the CAD subgroup showed a significant difference in terms of serum triglyceride levels (2.326 ± 1.889 vs 2.059 ± 1.447, p = 0.019). Analysis of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), apolipoprotein A (ApoA), and apolipoprotein B (ApoB) levels revealed no significant differences between the TT and CC + CT genotypes. Furthermore, no significant differences in serum lipid levels were observed between genotypes of the other SNPs. Multivariable logistic analysis, controlling for gender, age, body mass index (BMI), triglycerides (TG), TC, HDL-C, LDL-C, ApoA and ApoB, demonstrated that rs7257062 was still an independent risk factor of CAD (OR = 1.499, 95% CI: 1.036–2.168, p = 0.032). MDR analysis revealed that the rs7257062 interacted significantly with environmental factors such as smoking, diabetes, hypertension, BMI, and TG (p < 0.05). Conclusions: The rs7257062 variation of the C3 gene could be linked to both lipid balance and the risk of CAD. It is conceivable that the interplay between C3 polymorphisms and environmental elements could account for the etiology of CAD.

Background: Major depressive disorder (MDD) is known to be characterized by altered brain functional connectivity (FC) patterns. However, whether and how the features of dynamic FC would change in patients with MDD are unclear. In this study, we aimed to characterize dynamic FC in MDD using a large multi-site sample and a novel dynamic network-based approach. Methods: Resting-state functional magnetic resonance imaging (fMRI) data were acquired from a total of 460 MDD patients and 473 healthy controls, as a part of the REST-meta-MDD consortium. Resting-state dynamic functional brain networks were constructed for each subject by a sliding-window approach. Multiple spatio-temporal features of dynamic brain networks, including temporal variability, temporal clustering and temporal efficiency, were then compared between patients and healthy subjects at both global and local levels. Results: The group of MDD patients showed significantly higher temporal variability, lower temporal correlation coefficient (indicating decreased temporal clustering) and shorter characteristic temporal path length (indicating increased temporal efficiency) compared with healthy controls (corrected p < 3.14×10−3). Corresponding local changes in MDD were mainly found in the default-mode, sensorimotor and subcortical areas. Measures of temporal variability and characteristic temporal path length were significantly correlated with depression severity in patients (corrected p < 0.05). Moreover, the observed between-group differences were robustly present in both first-episode, drug-naïve (FEDN) and non-FEDN patients. Conclusions: Our findings suggest that excessive temporal variations of brain FC, reflecting abnormal communications between large-scale bran networks over time, may underlie the neuropathology of MDD.

To explore the alteration of global functional connectivity density (gFCD) in depressive patients after modified electroconvulsive therapy (MECT) and analyze the relationship between gFCD and clinical outcome. Thirty-seven subjects were evaluated based on the diagnostic criteria of the International Classification of Diseases-10 (ICD-10), consisting of a depressive group (24 patients after follow-ups) and a healthy control group with 13 normal individuals. All participants received Hamilton Depression Scale (HAMD) scores and resting-state functional magnetic resonance imaging scans. The gFCD significantly increased in the posterior-middle insula, the supra-marginal gyrus and the dorsal medial prefrontal cortex (dmPFC) before MECT treatment compared to healthy controlled patients. The gFCD statistically expanded in the perigenual anterior cingulate cortex (pgACC), the orbitofrontal cortex bilaterally and the left-supra-marginal gyrus after MECT, and it decreased notably in the posterior insula. The gFCD in the pgACC and the right orbital frontal cortex of depressive group before MECT showed a positive correlation with HAMD scores with treatment. Conforming to the impact of gFCD in depressive patients after MECT, the aforementioned brain region may become an indicator of MECT effect.

Objective. Electroconvulsive therapy (ECT) is considered one of the most effective and fast-acting treatment options for depressive episodes. Little is known, however, about ECT’s enabling brain (neuro)plasticity effects, particular for plasticity of white matter pathway. Materials and Methods. We collected longitudinal diffusion tensor imaging in the first-episode, drug-naïve major depressive disorder (MDD) patients n=24 before and after a predefined time window ECT treatment. We constructed large-scale anatomical networks derived from white matter fiber tractography and evaluated the topological reorganization using graph theoretical analysis. We also assessed the relationship between topological reorganization with improvements in depressive symptoms. Results. Our investigation revealed three main findings: (1) the small-worldness was persistent after ECT series; (2) anatomical connections changes were found in limbic structure, temporal and frontal lobes, in which the connection changes between amygdala and parahippocampus correlate with depressive symptom reduction; (3) significant nodal strength changes were found in right paralimbic network. Conclusions. ECT elicits neuroplastic processes associated with improvements in depressive symptoms that act to specific local ventral frontolimbic circuits, but not small-world property. Overall, ECT induced topological reorganization in large-scale brain structural network, opening up new avenues to better understand the mode of ECT action in MDD.