Protective effect of the apo epsilon2 allele in major depressive disorder in Taiwanese

OBJECTIVE: Major depression is an important comorbidity in Alzheimer's disease, which is definitely associated with the apolipoprotein E (apo E) polymorphism. The aim of this study was to explore the role of the different apo E polymorphisms in major depressive disorder (MDD) in a Taiwanese population. METHOD: We examined apo E genotypes in 273 Taiwanese patients with MDD and 429 healthy community controls, and compared their polymorphism distribution. RESULTS: The allelic frequency of apo epsilon2 was significantly lower in patients with MDD than in the controls, whereas no significant difference in apo epsilon4 allelic frequency between these two groups was found. CONCLUSION: The apo epsilon4 allele was not associated with MDD in this study. However, the finding of a lower frequency of the apo epsilon2 allele in MDD could lead to the conclusion that the apo epsilon2 allele likely provides a protective effect against MDD in the Taiwanese population.     

Personality disorder comorbidity in panic disorder patients with or without current major depression

To investigate the relationship between current or past major depressive disorder (MDD) on comorbid personality disorders in patients with panic disorder, we compared the comorbidity of personality disorders using the Structured Clinical Interview for DSM-III-R personality disorders (SCID-II) in 34 panic disorder patients with current MDD (current-MD group), 21 with a history of MDD but not current MDD (past-MD group), and 32 without lifetime MDD comorbidity (non-MD group). With regard to personality disorders, patients in the current-MD group met criteria for at least one personality disorder significantly more often than patients in the past-MD group or the non-MD group (82.4% vs. 52.4% and 56.3%, respectively). The current-MD group showed statistically significantly more borderline, dependent, and obsessive-compulsive personality disorders than the past-MD group or non-MD group. With stepwise regression analyses, number of MDD episodes emerged as an indicator of the comorbidity of cluster C personality disorder and any personality disorders. Future studies should determine whether aggressive treatment of comorbid personality disorders improves the outcome (e.g., lowers the likelihood of comorbid MDD) of patients with panic disorder.     

Tryptophan hydroxylase 2 gene is associated with major depression and antidepressant treatment response

Tryptophan hydroxylase-2 (TPH2) is the rate-limiting biosynthetic isoenzyme for serotonin that is preferentially expressed in the brain and has been implicated in the pathogenesis of major depressive disorder (MDD) and in the mechanism of antidepressant action. This study aimed to investigate whether common genetic variation in the TPH2 gene is associated with MDD and therapeutic response to antidepressants in a Chinese population. A total of 508 MDD patients and 463 unrelated controls were recruited. Among the MDD patients, 187 accepted selective serotonin reuptake inhibitor (fluoxetine or citalopram) antidepressant treatment for 8 weeks with therapeutic evaluation before and after treatment. Five TPH2 polymorphisms were genotyped and their association with MDD or treatment response was assessed by haplotype and single-marker analysis. In single-marker-based analysis, the rs17110747-G homozygote polymorphism was found to be more frequent in the MDD patients than in the controls (P = 0.002). Genotype analysis in responders (defined as those with a 50% reduction in baseline Hamilton score) and non-responders after 8 weeks of antidepressant treatment showed that the proportion of rs2171363 heterozygote carriers was higher in the responders than the non-responders (P = 0.009). No significant association with MDD or antidepressant therapeutic response was discovered in haplotype analyses. Our findings show that TPH2 genetic variants may play a role in MDD susceptibility and in acute therapeutic response to selective serotonin reuptake inhibitors.     

Incident and recurrent major depressive disorder and coronary artery disease severity in acute coronary syndrome patients

There is recent evidence that acute coronary syndrome (ACS) patients with first time incident major depressive disorder (MDD) and those with recurrent MDD represent different subtypes among individuals with ACS and comorbid depression. However, few studies have examined whether or not these subtypes differ in coronary artery disease (CAD) severity. We assessed whether those with incident MDD (in-hospital MDD and negative for history of MDD) or recurrent MDD (in-hospital MDD and a positive history of MDD) differ in angiographically documented CAD severity. Within 1 week of admission for ACS, 88 patients completed a clinical interview to assess current and past diagnosis of MDD. CAD severity was assessed in all patients by coronary angiography. A hierarchical regression analysis showed that neither in-hospital MDD status, nor history of MDD were significant predictors of CAD severity, but the interaction term between in-hospital MDD status and history of MDD was a significant predictor of CAD severity, after controlling for age, sex and ethnicity. Follow-up analyses showed that patients with first time, incident MDD had significantly more severe CAD compared to patients with recurrent MDD (p=0.043). To conclude, our study adds to the growing evidence that patients with incident MDD should be considered as a clinically distinct subtype from those with recurrent MDD. Possible mechanisms for differing CAD severity by angiogram between these two subtypes are proposed and implications for prognosis and treatment are discussed.     

Age at onset in 3014 Sardinian bipolar and major depressive disorder patients

Tondo L, Lepri B, Cruz N, Baldessarini RJ. Age at onset in 3014 Sardinian bipolar and major depressive disorder patients. Objective: To test if onset age in major affective illnesses is younger in bipolar disorder (BPD) than unipolar‐major depressive disorder (UP‐MDD), and is a useful measure. Method: We evaluated onset‐age for DSM‐IV‐TR major illnesses in 3014 adults (18.5% BP‐I, 12.5% BP‐II, 69.0% UP‐MDD; 64% women) at a mood‐disorders center. Results: Median and interquartile range (IQR) onset‐age ranked: BP‐I = 24 (19–32) < BP‐II = 29 (20–40) < UP‐MDD = 32 (23–47) years (P < 0.0001), and has remained stable since the 1970s. In BP‐I patients, onset was latest for hypomania, and depression presented earlier than in BP‐II or UP‐MDD cases. Factors associated with younger onset included: i) being unmarried, ii) more education, iii) BPD‐diagnosis, iv) family‐history, v) being employed, vi) ever‐suicidal, vii) substance‐abuse and viii) ever‐hospitalized. Onset‐age distinguished BP‐I from UP‐MDD depressive onsets with weak sensitivity and specificity. Conclusion: Onset age was younger among BPD than MDD patients, and very early onset may distinguish BPD vs. UP‐MDD with depressive‐onset.     

Indicators of pretreatment suicidal ideation in adults with major depressive disorder

Morris DW, Trivedi MH, Husain MM, Fava M, Budhwar N, Wisniewski SR, Miyahara S, Gollan JK, Davis LL, Daly EJ, Rush AJ. Indicators of pretreatment suicidal ideation in adults with major depressive disorder. Objective: In order to evaluate the presence of treatment emergent suicidal ideation (SI), it becomes necessary to identify those patients with SI at the onset of treatment. The purpose of this report is to identify sociodemographic and clinical features that are associated with SI in major depressive disorder (MDD) patients prior to treatment with a selective serotonin reuptake inhibitor. Method: This multisite study enrolled 265 out‐patients with non‐psychotic MDD. Sociodemographic and clinical features of participants with and without SI were compared post hoc. Results: Social phobia, bulimia nervosa, number of past depressive episodes, and race were independently associated with SI by one or more SI measure. Conclusion: Concurrent social phobia and bulimia nervosa may be potential risk factors for SI in patients with non‐psychotic MDD. Additionally, patients with more than one past depressive episode may also be at increased risk of SI.     

Intra-episode hypomanic symptoms during major depression and their correlates

Recent studies have shown that 40-50% of major depressive disorders (MDD) may become bipolar with time. Intra-episode hypomanic symptoms in MDD may be a first step in this shift. The purpose of the present study was to find factors associated with intra-episode hypomanic symptoms in MDD. Two hundred and forty-three consecutive MDD outpatients were interviewed with the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders (4th edn; DSM-IV), Clinician Version (SCID-CV), as modified by Benazzi and Akiskal (J. Affect. Disord. 2003; 73: 33-38). History of hypomania and presence of hypomanic symptoms during major depressive episode (MDE) were systematically assessed. Intra-episode hypomanic symptoms were defined as an MDE combined with three or more hypomanic symptoms, following Akiskal and Benazzi (J. Affect. Disord. 2003; 73: 113-122). Major depressive disorder with intra-episode hypomanic symptoms (MDD + H) was compared to MDD without hypomanic symptoms on classic bipolar validators. It was found that MDD + H (usually irritability, distractibility, racing thoughts, psychomotor agitation, and more talkativeness) was present in 32.5% of patients. Patients with MDD + H versus MDD had significantly lower age at onset, more atypical depressions, and more bipolar family history. Recurrences were not significantly different. Multivariate logistic regression found that bipolar family history and atypical depression were significantly and independently associated with MDD + H. Findings suggest that MDD + H may be associated with a bipolar vulnerability. Duration of illness and recurrences do not seem to be important for the onset of MDD + H. Bipolar genetic vulnerability seems to be required for onset of intra-episode hypomanic symptoms in MDD. Intra-episode hypomanic symptoms might be the first step of a process leading to the switch of MDD to bipolar disorders. Predicting the switch might have important treatment implications, because antidepressants used alone may worsen the course of bipolar disorders. Prospective studies are required to support these findings and hypotheses.     

Panic disorder versus panic disorder with major depression: Defining and understanding differences in psychiatric morbidity

The present study examined the impact of comorbid major depressive disorder (MDD) on psychiatric morbidity, panic symptomatology and frequency of other comorbid psychiatric conditions in subjects with panic disorder (PD). Four hundred thirty-seven patients with PD were evaluated at intake as part of a multicenter longitudinal study of anxiety disorders; 113 of these patients were also in an episode of MDD. Patients were diagnosed by DSM-III-R criteria utilizing structured clinical interviews. The 113 PD/MDD patients were compared with the 324 remaining PD subjects regarding panic symptoms at intake, sociodemographic, quality of life and psychiatric morbidity variables. Differences in frequency of other comorbid Axis I psychiatric disorders were assessed at intake; personality disorders were evaluated twelve months after intake. The results revealed that PD/MDD patients exhibit increased morbidity and decreased psychosocial functioning as compared to PD patients. Personality disorders were more prevalent in the PD/MDD group at six month follow-up assessment; the PD/MDD group also had an increased frequency of posttraumatic stress disorder (PTSD) and more comorbid Axis I anxiety disorders as compared to the PD group. The total number and frequency of panic symptoms was highly consistent between the two patient groups. Depression and Anxiety 5:12–20, 1997. © 1997 Wiley-Liss, Inc.     

Frequency-specific alterations in functional connectivity in treatment-resistant and -sensitive major depressive disorder

Major depressive disorder (MDD) may involve alterations in brain functional connectivity in multiple neural circuits and present large-scale network dysfunction. Patients with treatment-resistant depression (TRD) and treatment-sensitive depression (TSD) show different responses to antidepressants and aberrant brain functions. This study aims to investigate functional connectivity patterns of TRD and TSD at the whole brain resting state. Seventeen patients with TRD, 17 patients with TSD, and 17 healthy controls matched with age, gender, and years of education were recruited in this study. The brain was divided using an automated anatomical labeling atlas into 90 regions of interest, which were used to construct the entire brain functional networks. An analysis method called network-based statistic was used to explore the dysconnected subnetworks of TRD and TSD at different frequency bands. At resting state, TSD and TRD present characteristic patterns of network dysfunction at special frequency bands. The dysconnected subnetwork of TSD mainly lies in the fronto-parietal top-down control network. Moreover, the abnormal neural circuits of TRD are extensive and complex. These circuits not only depend on the abnormal affective network but also involve other networks, including salience network, auditory network, visual network, and language processing cortex. Our findings reflect that the pathological mechanism of TSD may refer to impairment in cognitive control, whereas TRD mainly triggers the dysfunction of emotion processing and affective cognition. This study reveals that differences in brain functional connectivity at resting state reflect distinct pathophysiological mechanisms in TSD and TRD. These findings may be helpful in differentiating two types of MDD and predicting treatment responses.     

Morphology of the corpus callosum in treatment‐resistant schizophrenia and major depression

Objective: To identify possible differences in the mean midsagittal corpus callosum (CC) total and subdivision areas in treatment‐resistant schizophrenia and depression (TRS and TRD) patients. Method: Areas of the total CC and its five equidistant subregions (from CC1 to CC5) obtained by parallel grid partitioning schemes were manually segmented from brain MRI of 42 TRS, 45 TRD patients and 30 healthy controls. The intracranial volume (ICV) normalized areas were calculated and compared between groups. Results: When compared with controls, patients with TRS had reduced ICV and a larger CC5, and TRD patients had a smaller CC4 while no significant difference in CC total area in patients with TRS or TRD was found. Multiple individual segments and total CC areas were significantly larger in TRS than TRD patients after normalization. Conclusion: Patients with TRS and TRD have different CC morphological characteristics, and therefore there may be aberrant interhemispheric connectivity in schizophrenia and major depressive disorder patients.     

S100B-immunopositive astrocytes and oligodendrocytes in the hippocampus are differentially afflicted in unipolar and bipolar depression: A postmortem study

Background

Previous studies have suggested that affective disorders are characterized by glial pathology. In this context, it has been hypothesized that elevated S100B serum and cerebrospinal fluid levels may represent a suitable surrogate marker. However, brain studies on the cellular distribution pattern of S100B in depressed patients are lacking so far. Such analyses are crucial, since S100B has been detected in various other cell types, even outside the central nervous system.

Methods

Therefore, we performed a first postmortem analysis on this topic in the hippocampus – which is of major importance for emotional and cognitive aspects of affective disorders. S100B-immunopositive astrocytes and oligodendrocytes were evaluated in the alveus and the CA1 pyramidal layer of patients with major depressive disorder (MDD) or bipolar I disorder (BD) compared to controls.

Results

As revealed by the optical disector cell-counting method, the numerical density of S100B-immunopositive astrocytes was bilaterally decreased in the CA1 pyramidal layer of MDD and BD patients compared to controls, whereas only the bipolar group showed a decreased density of S100B-immunopositive oligodendrocytes in the left alveus. These results were not confounded by gender, age, duration of disease, medication dosage, or autolysis time.

Conclusions

Confirming the idea of previous S100B serum and cerebrospinal fluid studies, our data suggest that S100B-immunopositive glia is dysregulated in the brains of depressed patients. These findings are in accordance with animal experiments in rodents showing a reduced astrocytic S100B-immunoreactivity in the hippocampus after pharmacological serotonin depletion (modeling depression).     

Neuropeptide Y in PTSD,MDD, and chronic stress: A systematic review and meta-analysis

Previous studies have suggested that neuropeptide Y (NPY) levels may be altered in patients with major depressive disorder (MDD), post-traumatic stress disorder (PTSD) and chronic stress. We investigated, through systematic review and meta-analysis, whether the mean levels of NPY are significantly different in patients with MDD, PTSD or chronic stress, compared to controls. The main outcome was the pooled standardized mean difference (SMD) with 95% confidence intervals between cases and controls, using the random-effects model. Heterogeneity and publication bias were evaluated. Thirty-five studies met eligibility criteria. Meta-regression determined that medication and sex could explain 27% of the between-study variance. Females and participants currently prescribed psychotropic medications had significantly higher levels of NPY. NPY levels were significantly lower in plasma and cerebrospinal fluid (CSF) in PTSD patients versus controls. Patients with MDD had significantly lower levels of NPY in plasma compared to controls, but not in the CSF. The magnitudes of the decrease in plasma NPY levels were not significantly different between PTSD and MDD. However, chronic stress patients had significantly higher plasma NPY levels compared to controls, PTSD or MDD. Our findings may imply a shared role of NPY in trauma and depression: nevertheless, it is not clear that the association is specific to these disorders. Psychotropic medications may help restore NPY levels. Further controlled studies are needed to better delineate the contribution of confounding variables such as type of depression, body mass index, appetite or sleep architecture.     

Cognition in older adults with bipolar disorder versus major depressive disorder

Gildengers AG, Butters MA, Chisholm D, Anderson SJ, Begley A, Holm M, Rogers JC, Reynolds CF III, Mulsant BH. Cognition in older adults with bipolar disorder versus major depressive disorder. Bipolar Disord 2012: 14: 198–205. © 2012 The Authors. Journal compilation © 2012 John Wiley & Sons A/S. Objectives: Bipolar disorder (BD) and major depressive disorder (MDD) are associated with cognitive dysfunction in older age during both acute mood episodes and remitted states. The purpose of this study was to investigate for the first time the similarities and differences in the cognitive function of older adults with BD and MDD that may shed light on mechanisms of cognitive decline. Methods: A total of 165 subjects with BD (n = 43) or MDD (n = 122), ages ≥ 65 years [mean (SD) 74.2 (6.2)], were assessed when euthymic, using comprehensive measures of cognitive function and cognitive–instrumental activities of daily living (C‐IADLs). Test results were standardized using a group of mentally healthy individuals (n = 92) of comparable age and education level. Results: Subjects with BD and MDD were impaired across all cognitive domains compared with controls, most prominently in Information Processing Speed/Executive Function. Despite the protective effects of having higher education and lower vascular burden, BD subjects were more impaired across all cognitive domains compared with MDD subjects. Subjects with BD and MDD did not differ significantly in C‐IADLs. Conclusion: In older age, patients with BD have worse overall cognitive function than patients with MDD. Our findings suggest that factors intrinsic to BD appear to be related to cognitive deterioration and support the understanding that BD is associated with cognitive decline.     

抑郁障碍患者家庭功能的跨文化研究

目的:探讨中国和美国抑郁障碍患者的家庭功能特征.方法:采用家庭功能量表(FAD)对92例中国抑郁障碍患者(中国组)及92例美国抑郁障碍患者(美国组)进行评估及比较.结果:两组FAD各维度均分均高于健康的家庭功能临界值,为不健康的家庭功能.中国组FAD中的情感反应维度评分及行为控制维度评分明显高于美国组;中国男性组情感反...     

Shared and distinct brain fMRI response during performance of working memory tasks in adult patients with schizophrenia and major depressive disorder

Working memory (WM) impairments are common features of psychiatric disorders. A systematic meta‐analysis was performed to determine common and disorder‐specific brain fMRI response during performance of WM tasks in patients with SZ and patients with MDD relative to healthy controls (HC). Thirty‐four published fMRI studies of WM in patients with SZ and 18 published fMRI studies of WM in patients with MDD, including relevant HC, were included in the meta‐analysis. In both SZ and MDD there was common stronger fMRI response in right medial prefrontal cortex (MPFC) and bilateral anterior cingulate cortex (ACC), which are part of the default mode network (DMN). The effects were of greater magnitude in SZ than MDD, especially in prefrontal‐temporal‐cingulate‐striatal‐cerebellar regions. In addition, a disorder‐specific weaker fMRI response was observed in right middle frontal gyrus (MFG) in MDD, relative to HC. For both SZ and MDD a significant correlation was observed between the severity of clinical symptoms and lateralized fMRI response relative to HC. These findings indicate that there may be common and distinct anomalies in brain function underlying deficits in WM in SZ and MDD, which may serve as a potential functional neuroimaging‐based diagnostic biomarker with value in supporting clinical diagnosis, measuring illness severity and assessing the efficacy of treatments for SZ and MDD at the brain level.     

Elevated levels of cerebrospinal fluid neuron-specific enolase (NSE), but not S100B in major depressive disorder

Objectives. Alterations in neuronal and glial integrity are considered to be of pathogenic impact on major depressive disorder (MDD). For MDD, data on cerebrospinal fluid (CSF) levels of neuron-specific enolase (NSE) are lacking and scarce for glial protein S100B. Methods. We measured CSF levels of NSE and S100B in 31 patients with MDD and 32 mentally healthy controls using electrochemiluminescence immunoassays (ECLIA). Results. Adjusted means of NSE were significantly elevated in the MDD patients (11.73 ng/ml (9.95–13.52 95% CI) compared to the controls (6.17 ng/ml (4.55–7.78), F = 9.037, P = 0.004. Effect size for adjusted mean group difference of 5.57 ng/ml was found invariably high (Cohen’s d = 1.23). Differentiating MDD from controls, a NSE cut-off of 7.94 ng/ml showed sensitivity of 81% (95% CI 63.7–90.8) and specificity of 75% (95% CI 57.9–86.7). Adjusted levels of S100B did not differ significantly between the two groups (1.12 ng/ml (0.77–1.48) in MDD, 0.97 ng/ml (0.64–1.30) in controls). Conclusions. Our results of elevated CSF-NSE levels support neuronal pathology in MDD and the potential use of CSF-NSE as marker in clinical diagnostics. Missing group differences in S100B do not promote a specific glial pathology in depressive disorders.     

Effects of venlafaxine and fluoxetine on lymphocyte subsets in patients with major depressive disorder: A flow cytometric analysis

Background

Studies have yielded conflicting results concerning flow cytometric lymphocyte analyses in patients with depression. Data about the effect of antidepressants on lymphocyte subsets are also contradictory. The aim of this study was to determine effects of venlafaxine versus fluoxetine on lymphocyte subsets in depressive patients.

Methods

Sixty-nine patients diagnosed with major depressive disorder (MDD) according to DSM-IV and 36 healthy controls are included in the study. Sixty-nine patients were randomized to take fluoxetine (FLX) (n = 33) or venlafaxine (VEN) (n = 36). Serum lymphocyte subsets included CD3, CD4, CD8, CD16/56, CD19, CD45, Anti-HLA-DR which were measured by flow cytometric analyses at baseline and 6 weeks after the start of treatment. The severity of depression was evaluated with Hamilton rating scale for depression.

Results

At baseline, patients with MDD had significantly lower CD16/56 ratio and higher CD45 ratio compared to the controls. Although numerically higher in the VEN treated patients, treatment response rates between the FLX (53%) and the VEN (75%) groups were not different statistically. CD45 values decreased significantly in the VEN group at the end of the 6 week treatment period whereas no difference was observed in the FLX group. By the 6th week, treatment responders showed a significantly higher CD16/56 ratio than non-responders. Baseline severity of depression and anxiety was positively correlated with baseline CD45 ratio and negatively correlated with baseline CD16/56 ratio. We did not observe consistent changes in the absolute number of circulating B or T cells, nor in the helper/inducer (CD4) or suppressor/cytotoxic (CD8) subsets.

Conclusions

CD16/56 was lower in patients with MDD and increased in treatment responders at 6th week. CD45 ratio was higher in patients with MDD than healthy subjects; it decreased with antidepressant treatment and was positively correlated with the severity of depression. Antidepressant treatment contributes to immune regulation in patients with major depressive disorder.     

Self‐esteem in remitted bipolar disorder patients: a meta‐analysis

Nilsson KK, Jørgensen CR, Craig TKJ, Straarup KN, Licht RW. Self‐esteem in remitted bipolar disorder patients: a meta‐analysis.
Bipolar Disord 2010: 12: 585–592. © 2010 The Authors.
Journal compilation © 2010 John Wiley & Sons A/S. Objectives: Low self‐esteem has been found to be a risk factor for depression in major depressive disorder (MDD). In contrast, the role of self‐esteem in bipolar disorder (BD) is still uncertain. In order to examine the characteristics of self‐esteem in BD, we synthesized studies comparing self‐esteem in BD patients with self‐esteem in MDD patients and in normal controls. Methods: Database searches and identification of studies were conducted by two of the authors independently. Remission of BD and MDD was a major selection criterion. The results were generated through meta‐analyses. Results: Random‐effects models of 19 between‐group comparisons (N = 1,838) suggested that the self‐esteem of remitted BD patients was significantly lower than that of normal controls (Cohen’s d = ?0.83), while significantly higher than that of remitted MDD patients (Cohen’s d = 0.54). Fail‐safe numbers and tests for funnel plot asymmetry indicated that the results were robust and unlikely to reflect publication biases. Additional studies indicated that self‐esteem may take a fluctuating course during remission of BD. Conclusions: By revealing that BD patients do experience low self‐esteem, the findings implicate a need for further understanding the causes and therapeutic impact of such abnormality in BD.     

Treatment resistant depression as a failure of brain homeostatic mechanisms: Implications for deep brain stimulation

Given the profound negative public health effects of major depressive disorder (MDD), and data suggesting only modest effectiveness of existing psychological and pharmacological treatments for this condition, there has been increasing interest in exploring the antidepressant potential of non-pharmacological, brain-based interventions, such as deep brain stimulation (DBS). The use of the DBS for psychiatric indications follows a decade of data suggesting that DBS is an effective, evidence-based strategy for the treatment of movement disorders such as Parkinson's disease. At the present time there is open-label case series data to suggest that DBS in the subgenual cingulate gyrus, ventral caudate/ventral striatum, and the nucleus accumbens, is associated with antidepressant effects in individuals who fail to respond to conventional treatments for MDD. However a number of unresolved issues about the optimal use of DBS for MDD remain, such as the optimal anatomical placement of the electrodes and the mechanisms of its antidepressant effects. This review summarizes the clinical experience of DBS for treatment resistant depression (TRD). The rationale for the use of DBS for TRD is reviewed in the context of the growing neuroimaging literatures exploring the biomarkers of antidepressant response, and the neural substrates of emotional regulation in both normal and pathological states.     

Higher serum VGF protein levels discriminate bipolar depression from major depressive disorder

Misdiagnosis between major depressive disorder (MDD) and bipolar depression (BD) is quite common. Our previous study found significantly lower serum VGF (non-acronymic) in MDD patients. However, it is unclear whether same changes occur in BD patients. Therefore, we aimed to investigate the relationship between serum VGF levels in BD and MDD patients. General information, scores of 17-item Hamilton Depression Rating Scale (HDRS), and fasting blood samples of all participants including 30 MDD patients, 20 BD patients, and 30 healthy controls (HC) were collected. Serum VGF levels were measured by Enzyme-linked immunosorbent assay kits. Pearson correlation analysis was used to analyze correlations between serum VGF levels and clinical information. Receiver operating characteristic (ROC) curve and likelihood ratios (LRs) were used to analyze the differential potential of serum VGF. Serum VGF levels were significantly lower in MDD patients but higher in BD patients compared with HC (both P_Tukey < 0.01). No correlation was found between serum VGF levels and any data of subjects. The optimal cutoff for serum VGF in discriminating BD patients from MDD patients was ≥1093.85 pg/ml (AUC = 0.990, sensitivity of 95%, specificity of 100% and accuracy of 95%). LRs further confirmed the differential efficiency of serum VGF in distinguishing BD and MDD patients with +LR of infinity and –LR of 0. The results suggest that serum VGF level changed significantly in MDD and BD patients and serum VGF may be an indicator for differentiating BD patients from MDD patients.