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Studies have suggested that depression was accompanied by oxidative stress dysregulation, including abnormal total antioxidant capacity (TAC), antioxidants, free radicals, oxidative damage and autoimmune response products. This meta-analysis aims to analyse the clinical data quantitatively by comparing the oxidative stress markers between depressed patients and healthy controls. A search was conducted to collect the studies that measured the oxidative stress markers in depressed patients. Studies were searched in Embase, Medline, PsychINFO, Science direct, CBMDisc, CNKI and VIP from 1990 to May 2015. Data were subjected to meta-analysis by using a random effects model for examining the effect sizes of the results. Bias assessments, heterogeneity assessments and sensitivity analyses were also conducted. 115 articles met the inclusion criteria. Lower TAC was noted in acute episodes (AEs) of depressed patients (p<0.05). Antioxidants, including serum paraoxonase, uric acid, albumin, high-density lipoprotein cholesterol and zinc levels were lower than controls (p<0.05); the serum uric acid, albumin and vitamin C levels were increased after antidepressant therapy (p<0.05). Oxidative damage products, including red blood cell (RBC) malondialdehyde (MDA), serum MDA and 8-F2-isoprostanes levels were higher than controls (p<0.05). After antidepressant medication, RBC and serum MDA levels were decreased (p<0.05). Moreover, serum peroxide in free radicals levels were higher than controls (p<0.05). There were no differences between the depressed patients and controls for other oxidative stress markers. This meta-analysis supports the facts that the serum TAC, paraoxonase and antioxidant levels are lower, and the serum free radical and oxidative damage product levels are higher than controls in depressed patients. Meanwhile, the antioxidant levels are increased and the oxidative damage product levels are decreased after antidepressant medication. The pathophysiological relationships between oxidative stress and depression, and the potential benefits of antioxidant supplementation deserve further research.

Background Evidence suggests that alterations in serum trace element concentrations are closely associated with mental illness. However, ​studies on the relationship between serum copper, zinc, and selenium concentrations and depressive symptoms are limited and with controversial results. We aimed to investigate the association between serum concentrations of these trace elements and depressive symptoms in US adults. Methods Data from the National Health and Nutrition Examination Survey (NHANES) (2011–2016) were used in this cross-sectional study. The Patient Health Questionnaire-9 Items (PHQ-9) was employed to assess depressive symptoms. Multiple logistic regression was performed to determine the relationship between the serum concentrations of copper, zinc, and selenium and depressive symptoms. Results A total of 4552 adults were included. Subjects with depressive symptoms had higher serum copper concentrations (123.88 ± 1.87) than those without depressive symptoms (116.99 ± 0.86) ( p  < 0.001). In Model 2, weighted logistic regression analysis showed that the second (Q2) quartile of zinc concentrations (odds ratio [OR] = 1.534, 95% confident interval [CI]: 1.018 to 2.313) were significantly associated with an increased risk of depressive symptoms. Subgroup analysis revealed that the third (Q3) and fourth (Q4) quartiles of copper concentrations (Q3: OR = 2.699, 95% CI: 1.285 to 5.667; Q4: OR = 2.490, 95% CI: 1.026 to 6.046) were also positively associated with depressive symptoms in obese individuals after controlling for all confounders. However, no significant relationship between serum selenium concentrations and depressive symptoms was observed. Conclusions Obese US adults with high serum copper concentrations, as well as US adults in general with low serum zinc concentrations, were susceptible to depressive symptoms. Nevertheless, the causal mechanisms underlying these relationships need to be further explored.

The relationships of the gut microbiota-inflammation-brain axis in depressive bipolar disorder (BD) remains under-elaborated. Sixty-five unmedicated depressive patients with BD II and 58 controls (HCs) were prospectively enrolled. Resting-state functional MRI data of static and dynamic amplitude of low-frequency fluctuation (ALFF) was measured, and abnormal ALFF masks were subsequently set as regions of interest to calculate whole-brain static functional connectivity (sFC) and dynamic functional connectivity (dFC). Fecal samples were collected to assess gut diversity and enterotypes using 16S amplicon sequencing. Blood samples were also collected, serum was assayed for levels of cytokines (interleukin [IL]-2, IL-4, IL-6, IL-8, IL-10, tumor necrosis factor [TNF]-α). Patients with BD II exhibited decreased static ALFF values in the left cerebellum Crus II, and decreased cerebellar sFC and dFC to the right inferior parietal lobule and right superior frontal gyrus, respectively. Moreover, higher pro-inflammatory and anti-inflammatory cytokines levels, and increased proinflammatory bacteria and glutamate and gamma-aminobutyric acid metabolism related bacteria were identified in BD II. The interaction of Parabacteroides levels × IL-8 levels was an independent contributor to static ALFF in the left cerebellar Crus II. The findings bridged a gap in the underlying pathophysiological mechanism of the gut microbiota-inflammation-brain axis in BD II depression.

Accumulating evidence has revealed the gut bacteria dysbiosis and brain hippocampal functional and structural alterations in major depressive disorder (MDD). However, the potential relationship between the gut microbiota and hippocampal function alterations in patients with MDD is still very limited. Data of resting-state functional magnetic resonance imaging were acquired from 44 unmedicated MDD patients and 42 demographically matched healthy controls (HCs). Severn pairs of hippocampus subregions (the bilateral cornu ammonis [CA1-CA3], dentate gyrus (DG), entorhinal cortex, hippocampal–amygdaloid transition area, and subiculum) were selected as the seeds in the functional connectivity (FC) analysis. Additionally, fecal samples of participants were collected and 16S rDNA amplicon sequencing was used to identify the altered relative abundance of gut microbiota. Then, association analysis was conducted to investigate the potential relationships between the abnormal hippocampal subregions FC and microbiome features. Also, the altered hippocampal subregion FC values and gut microbiota levels were used as features separately or together in the support vector machine models distinguishing the MDD patients and HCs. Compared with HCs, patients with MDD exhibited increased FC between the left hippocampus (CA2, CA3 and DG) and right hippocampus (CA2 and CA3), and decreased FC between the right hippocampal CA3 and bilateral posterior cingulate cortex. In addition, we found that the level of proinflammatory bacteria (i.e., Enterobacteriaceae ) was significantly increased, whereas the level of short-chain fatty acids producing-bacteria (i.e., Prevotellaceae, Agathobacter and Clostridium ) were significantly decreased in MDD patients. Furthermore, FC values of the left hippocampal CA3- right hippocampus (CA2 and CA3) was positively correlated with the relative abundance of Enterobacteriaceae in patients with MDD. Moreover, altered hippocampal FC patterns and gut microbiota level were considered in combination, the best discrimination was obtained (AUC = 0.92). These findings may provide insights into the potential role of gut microbiota in the underlying neuropathology of MDD patients.

Bipolar disorder (BD) is frequently misdiagnosed as major depressive disorder (MDD) in clinical practice, especially during depressive episodes. A unifying triple-network model, involving the default mode network (DMN), central executive network (CEN) and salience network (SN), has been proposed to explain the neural physiopathology of psychiatric and neurological disorders. Although several studies revealed shared and specific alterations between BD and MDD in key regions of DMN, CEN, and SN, and a few studies used different measures to detect detailed alterations in the triple networks in BD and MDD, their shared and specific patterns of altered functional connectivity (FC) in the triple networks has remained unclear. In this study, we acquired resting-state fMRI (R-fMRI) data from 38 unmedicated BD and 35 unmedicated MDD patients during depressive episodes along with 47 healthy controls. We first determined the spatially independent components of the DMN, SN, and CEN by using independent component analysis (ICA); then we estimated the inter-ROI and inter-network FC for each group. By comparing the differences between the three groups, we obtained the following results: (1) both the BD and MDD patients showed shared weaker intra-network FC in the left mPFC and right precuneus within the DMN as well as weaker inter-ROI FC between the left AI and right AI compared with the healthy controls; (2) the BD had weaker while the MDD had stronger intra-network FC in the right dlPFC within the rCEN as well as stronger inter-ROI FC between the right dlPFC and right ANG compared with the healthy controls; (3) the BD showed specific, stronger inter-ROI FC between the left PPC and right AI as well as stronger inter-network FC between the lCEN and SN compared with either the MDD or the control group. Our findings provide new information for understanding the neural physiopathology and clinical symptoms of depressed BD and MDD patients.

Identifying brain differences and similarities between bipolar disorder (BD) and major depressive disorder (MDD) is necessary for increasing our understanding of the pathophysiology and for developing more effective treatments. However, the features of whole-brain intrinsic functional connectivity underlying BD and MDD have not been directly compared. We collected resting-state fMRI data from 48 BD patients, 48 MDD patients, and 51 healthy subjects. We constructed voxel-wise whole-brain functional networks and computed regional functional connectivity strength (FCS) using graph-theory and further divided the regional FCS into long-range FCS (lFCS) and short-range FCS (sFCS). Relative to the controls, both the BD and MDD patients showed decreased sFCS in the bilateral precuneus. In addition, the BD patients showed increased and the MDD patients showed decreased lFCS and sFCS in the bilateral cerebellum. The BD patients also showed increased lFCS in the right middle temporal gyrus and increased sFCS in the bilateral thalamus compared to either the MDD patients or the controls. These findings suggest that BD and MDD may have some shared as well as a greater number of specific impairments in their functional connectivity patterns, providing new evidence for the pathophysiology of BD and MDD at the large-scale whole brain connectivity level.

Background. Middle-aged (45-59 years old) patients with major depressive disorder (MDD) have a predilection for dementia and cognitive disorders (CDs); however, the characteristics and mechanisms of CDs in these patients remain unclear. There are also known connections between thyroid-stimulating hormone (TSH), brain biochemical metabolism, and cognitive function (CF); however, there is scanty of information about these connections in middle-aged MDD patients. Methods. Cognitive assessment was performed on 30 first-episode, untreated middle-aged patients with MDD and 30 well-matched healthy controls (HCs) using the MATRICS Consensus Cognitive Battery (MCCB). N-acetyl aspartate (NAA)/creatine (Cr) and choline (Cho)/Cr ratios in the prefrontal cortex (PFC) and cerebellum were also obtained via proton magnetic resonance spectroscopy (1H-MRS), and the TSH level was measured by chemiluminescence analysis. Results. MDD patients presented significantly lower processing speed, working memory, verbal learning, reasoning problem-solving, visual learning, and composite cognition scores than controls, with a statistically lower NAA/Cr ratio in the right cerebellum. Age was positively related to reasoning problem-solving in the MDD group (r=0.6249, p=0.0220). Education also showed a positive association with visual learning, social cognition, and composite cognition. The 24-item Hamilton Depression Rating Scale (HDRS-24) score was negatively related to all domains of CF. TSH levels were markedly decreased in the MDD group, and a positive connection was determined between the NAA/Cr ratio in the right PFC and the TSH level. Conclusions. Middle-aged MDD patients have multidimensional CDs. There are changes in PFC and cerebellar biochemical metabolism in middle-aged patients with MDD, which may be related to CDs or altered TSH levels.

Background This study aimed to characterise neurometabolic differences between bipolar disorder I (BD-I) and bipolar disorder II (BD-II), and to examine their associations with cognitive function. Methods A total of 50 patients diagnosed with BD-I, 80 patients with BD-II, and 50 healthy controls (HCs) were recruited for this study. Metabolite concentrations—specifically N-acetylaspartate (NAA) and choline-containing compounds (Cho)—were measured in the prefrontal white matter (PWM), anterior cingulate cortex (ACC), and thalamus through proton magnetic resonance spectroscopy (¹H-MRS). Cognitive performance was evaluated using the MATRICS Consensus Cognitive Battery (MCCB). Results When compared to HCs, patients with BD-II showed significantly higher Cho/Cr ratios in the right PWM and left ACC, along with lower NAA/Cr ratios in the right thalamus; compared to BD-II patients, those with BD-I exhibited higher Cho/Cr ratios in the right PWM and lower NAA/Cr ratios in the right thalamus; among BD-I patients, the Cho/Cr ratio in the left ACC was negatively correlated with measures of information processing speed and attentional vigilance. Conclusions This study demonstrates that BD-II patients exhibit greater cholinergic dysregulation in the left ACC and the right PWM, whereas BD-I patients show more pronounced neuronal dysfunction in the right thalamus. Furthermore, the left ACC Cho/Cr ratio was specifically associated with cognitive impairments in information processing speed and attentional vigilance, but only among patients with BD-I. This suggests that subtype-specific mechanisms underlie the relationship between neurometabolic abnormalities and cognitive deficits. Clinical trial number Not applicable.

Background The clinical characteristics of major depressive disorder (MDD) in adolescents show notable gender-related differences, but the cause of these differences is still not understood. The current research concentrates on the changes in neurometabolism and neuroendocrine function, aiming to identify differences in endocrine function and brain metabolism between male and female adolescents with MDD. Methods A total of 121 teenagers diagnosed with MDD (43 males and 78 females) were enlisted as participants. Measurement was conducted on levels of endocrine hormones, which included free tri-iodothyronine (FT3), total tri-iodothyronine (TT3), free thyroxin (FT4), total thyroxin (TT4), thyroid-stimulating hormone (TSH), cortisol, and adrenocorticotropic hormone (ACTH). Obtained through 1 H-MRS, the N-acetyl aspartate (NAA) and choline containing compounds (Cho) to creatine (Cr) ratios were acquired for the prefrontal whiter matter (PWM), anterior cingulate cortex (ACC), basal ganglia (BG), thalamus, and cerebellum. Result After adjusting for multiple comparisons, female adolescents with MDD showed lower ACTH levels compared to their male counterparts. An increased lateralization index (LI) was observed in female patients for both the thalamic Cho/Cr ratio and the basal ganglia NAA/Cr ratio. Additionally, an intriguing finding was that in male adolescent patients, TT4 levels were significantly correlated with the Cho/Cr ratio in the left cerebellum. However, no such correlation between hormones and brain metabolism was found in females. Conclusions Gender differences in endocrine and neurometabolic abnormalities may contribute to the gender-specific pathophysiology of MDD in adolescent patients. Metabolic abnormalities and lateralization changes are observed in different brain regions for male and female MDD patients.

Background Recent evidences have shown sex-differential cognitive deficits in bipolar disorder (BD) and differences in cognitions across BD subtypes. However, the sex-specific effect on cognitive impairment in BD subtype II (BD-II) remains obscure. The aim of the current study was to examine whether cognitive deficits differ by gender in youth with BD-II depression. Method This cross-sectional study recruited 125 unmedicated youths with BD-II depression and 140 age-, sex-, and education-matched healthy controls (HCs). The Chinese version of the Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS) Consensus Cognitive Battery (MCCB) was used to assess cognitive functions. Mood state was assessed using the 24-item Hamilton Depression Rating Scale (24-HDRS) and the Young Mania Rating Scale (YMRS). Multivariate analysis of covariance (MANCOVA) was conducted. Result ​Compared with HCs, patients with BD-II depression had lower scores on MCCB composite and its seven cognitive domains (all p  < 0.001). After controlling for age and education, MANCOVA revealed significant gender-by-group interaction on attention/vigilance (F = 6.224, df = 1, p  = 0.013), verbal learning (F = 9.847, df = 1, p  = 0.002), visual learning (F = 4.242, df = 1, p  = 0.040), and composite (F = 8.819, df = 1, p  = 0.003). Post hoc analyses suggested that males performed worse in the above-mentioned MCCB tests than females in BD-II depression. Conclusion Our study demonstrated generalized cognitive deficits in unmedicated youths with BD-II depression. Male patients performed more serious cognitive impairment on attention/vigilance, verbal learning, and visual learning compared to female patients.