Prefrontal cortex activities during verbal fluency and emotional words tasks in major depressive, adjustment, and bipolar disorders with depressive states.

Background: It can be difficult to differentiate psychiatric disorders from depressive states, with little knowledge on how to differentiate them. This study aimed to evaluate changes in brain activity during cognitive and emotional tasks in patients with depressive state to help with differential diagnoses.

Methods: Sixty-two patients with depressive states [17 with adjustment disorder (AD), 27 with major depressive disorder (MDD), and 18 with bipolar disorder (BD)] and 34 healthy controls (HC) were recruited.

Altered Connectivity of the Anterior Cingulate and the Posterior Superior Temporal Gyrus in a Longitudinal Study of Later-life Depression.

Patients with later-life depression (LLD) show abnormal gray matter (GM) volume, white matter (WM) integrity and functional connectivity in the anterior cingulate cortex (ACC) and posterior superior temporal gyrus (pSTG), but it remains unclear whether these abnormalities persist over time. We examined whether structural and functional abnormalities in these two regions are present within the same subjects during depressed vs. remitted phases.

Differences in frontotemporal dysfunction during social and non-social cognition tasks between patients with autism spectrum disorder and schizophrenia.

Although literature evidence suggests deficits in social and non-social cognition in patients with autistic spectrum disorder (ASD) and schizophrenia (SCZ), the difference in neural correlates of the impairments between the two disorders has not been elucidated. We examined brain function in response to a non-social cognition and a social cognition task using functional near-infrared spectroscopy (fNIRS) in 13 patients with ASD, 15 patients with SCZ, and 18 healthy subjects. We assessed the brain function of participants using a verbal fluency task and an emotional facial recognition task.

Altered plasma protein glycosylation in a mouse model of depression and in patients with major depression.

Background: Glycosylation is a common posttranslational modification in protein biosynthesis that is implicated in several disease states. It has been reported that specific protein glycan structures are useful as biomarkers for cancer and some neuropsychiatric diseases; however, the relationship between plasma protein glycosylation and major depressive disorder (MDD) has not been investigated to date. The aim of this study was to determine whether plasma protein glycan structures are altered in depression using a stress-based mouse model and samples from patients with MDD.

Disconnectivity between Dorsal Raphe Nucleus and Posterior Cingulate Cortex in Later Life Depression.

The dorsal raphe nucleus (DRN) has been repeatedly implicated as having a significant relationship with depression, along with its serotoninergic innervation. However, functional connectivity of the DRN in depression is not well understood. The current study aimed to isolate functional connectivity of the DRN distinct in later life depression (LLD) compared to a healthy age-matched population.

Identification of commonly altered genes between in major depressive disorder and a mouse model of depression.

The heterogeneity of depression (due to factors such as varying age of onset) may explain why biological markers of major depressive disorder (MDD) remain uncertain. We aimed to identify gene expression markers of MDD in leukocytes using microarray analysis. We analyzed gene expression profiles of patients with MDD (age ≥50, age of depression onset <50) (N = 10, depressed state; N = 13, remitted state).

Distinct and Shared Endophenotypes of Neural Substrates in Bipolar and Major Depressive Disorders.

Little is known about disorder-specific biomarkers of bipolar disorder (BD) and major depressive disorder (MDD). Our aim was to determine a neural substrate that could be used to distinguish BD from MDD. Our study included a BD group (10 patients with BD, 10 first-degree relatives (FDRs) of individuals with BD), MDD group (17 patients with MDD, 17 FDRs of individuals with MDD), and 27 healthy individuals.

Disrupted orbitomedial prefrontal limbic network in individuals with later-life depression.

Background: Depression in old age is an increasing contributor to poor health and accompanying health care costs. Although there is an abundance of literature on later-life depression (LLD), the neural correlates have not been clarified. The aim of this study was to determine whether patients with LLD show abnormal gray matter volume (GMV) and white matter integrity by using multiple image analysis methods.

Precentral and inferior prefrontal hypoactivation during facial emotion recognition in patients with schizophrenia: A functional near-infrared spectroscopy study.

Although patients with schizophrenia demonstrate abnormal processing of emotional face recognition, the neural substrates underlying this process remain unclear. We previously showed abnormal fronto-temporal function during facial expression of emotions, and cognitive inhibition in patients with schizophrenia using functional near-infrared spectroscopy (fNIRS). The aim of the current study was to use fNIRS to identify which brain regions involved in recognizing emotional faces are impaired in patients with schizophrenia, and to determine the neural substrates underlying the response to emotional facial expressions per se, and to facial expressions with cognitive inhibition.

Blunted brain activation in patients with schizophrenia in response to emotional cognitive inhibition: a functional near-infrared spectroscopy study.

Introduction: Patients with schizophrenia (SZ) have deficits of facial emotion processing and cognitive inhibition, but the brain pathophysiology underlying these deficits and their interaction are not clearly understood. We tested brain activity during an emotional face go/no-go task that requires rapid executive control affected by emotional stimuli in patients with SZ using functional near-infrared spectroscopy (fNIRS).

Methods: Twenty-five patients with SZ and 28 healthy control subjects were studied.

Different and shared brain volume abnormalities in late- and early-onset schizophrenia.

The differences in clinical characteristics between late- (LOS) and early-onset schizophrenia (EOS) are well documented. However, very little is known about the neural mechanisms underlying these differences. Here, we compared morphometric abnormalities between patients with EOS and those with LOS.

[Clinical examination of 3 patients with delayed neuropsychiatric encephalopathy induced by carbon monoxide poisoning, who recovered from severe neurocognitive impairment by repetitive hyperbaric oxygen therapy].

We performed hyperbaric oxygen (HBO) therapy for 3 patients with delayed neuropsychiatric encephalopathy induced by carbon monoxide (CO) poisoning. All patients were male and around 50 years old, and they had not received HBO therapy within 24 h after CO poisoning, even though they showed severe consciousness disturbance. In these patients, delayed neuropsychiatric encephalopathy appeared about 25 days after acute CO poisoning, and HBO therapy was initiated within 8 days after disease onset.

Prefrontal activation in response to emotional words in patients with bipolar disorder and major depressive disorder.

Abnormal emotional processing is involved in the pathophysiology of bipolar disorder (BD) and major depressive disorder (MDD). However, whether the neural mechanism underlying this deficit is a trait characteristic of BD and MDD is unclear. The aim of this study was to elucidate the similarities and differences in processing of emotional stimuli between patients with BD and MDD in remission, using functional near-infrared spectroscopy (fNIRS).

[Functional biomarkers of mood disorders: differential diagnosis and clinical classification with gene expression in peripheral leukocytes].

In order to identify the possible biomarkers of mood disorders, we measured the mRNA levels for a variety of genes in peripheral leukocytes of mood disorder patients in a depressive, as well as in a remissive state, comparing with healthy controls. We selected and measured the levels of genes of interest, which are listed as follows: glucocorticoid receptor, neurotrophic factors, cell adhesion molecules, SR protein splicing factors, transcription factors, epigenetic factors (histone deacetylase, sirtuin, DNA methyltransferase), since these molecules are suggested to be associated with the neural function, synaptic plasticity, and behaviors in animal models, as well as with the pathophysiology and pathogenesis of mood disorders. We found the three different types of biological markers: 1) state markers those revealed alterations of gene expression only in a depressive state of major depressive patients and/or bipolar depressive patients, 2) trait markers those showed altered gene expression both in a depressive and a remissive state of major depressive patients and/or bipolar depressive patients, and 3) markers of the treatment resistance those revealed different alterations of gene expression between treatment resistant and treatment responsive patients in a depressive state.

Neural correlates of plasma acylated ghrelin level in individuals with major depressive disorder.

Anhedonic symptoms, which include loss of pleasure, appetite and motivation, are key symptoms of major depressive disorder (MDD) and are thought to depend on a neural circuit of the mesolimbic system. The neuropeptide ghrelin plays a crucial role in appetite and reward. Little is known, however, about the role of ghrelin in MDD.

Reduced expression of glyoxalase-1 mRNA in mood disorder patients.

Glyoxalase-1 (Glo1) is an antioxidant enzyme which detoxifies alpha-ketoaldehydes to prevent the accumulation of pro-oxidant compounds, such as methylglyoxal, in all cell types. Glo1 has been suggested to be involved in anxiety disorders, autism, and Alzheimer's disease. Mood disorders have a high rate of comorbidity with anxiety disorders although, to date, little is known of the involvement of Glo1 in the pathophysiology of these conditions.

Characterization of the vulnerability to repeated stress in Fischer 344 rats: possible involvement of microRNA-mediated down-regulation of the glucocorticoid receptor.

In the present study, we established and characterized an animal model of vulnerability to repeated stress. We found that control Sprague-Dawley (SD) rats showed a gradual decrease in the HPA axis response following 14 days of repeated restraint stress, whereas Fischer 344 (F344) rats did not show such HPA axis habituation. Similar habituation was observed in the expression of c-fos mRNA, corticotropin-releasing hormone hnRNA, and phospho-CREB and phospho-ERK proteins in the hypothalamic paraventricular nucleus (PVN) of SD rats, but not in the F344 rats.

State-dependent changes in the expression levels of NCAM-140 and L1 in the peripheral blood cells of bipolar disorders, but not in the major depressive disorders.

Recent postmortem brain and imaging studies provide evidence for disturbances of structural and synaptic plasticity in patients with mood disorders. Several lines of evidence suggest that the cell adhesion molecules (CAMs), neural cell adhesion molecules (NCAM) and L1, play important roles in both structural and synaptic plasticity. Although postmortem brain studies have indicated altered expression levels of NCAM and L1, it is still unclear whether these changes are state- or trait-dependent.

Altered expression of neurotrophic factors in patients with major depression.

There is an abundance of evidence suggesting the involvement of altered levels of expression of neurotrophic factors in the pathophysiology of neuropsychiatric disorders. Although postmortem brain studies have indicated the alterations in the expression levels of neurotrophic factors in mood disorder patients, it is unclear whether these changes are state- or trait-dependent. In this study, we examined the expression levels of the members of the glial cell line-derived neurotrophic factor (GDNF) family (GDNF, artemin (ARTN), neurturin, and persephin), brain-derived neurotrophic factor, nerve growth factor, neurotrophin-3 (NT-3), and neurotrophin-4 mRNAs by using quantitative real-time PCR method in peripheral blood cells of patients with major depressive and bipolar disorders in both a current depressive and a remissive states.

Increased expression of splicing factor SRp20 mRNA in bipolar disorder patients.

Background: Variations and defects in alternative splicing are well known to be associated with a variety of human diseases and the stress response. We previously reported a decrease in glucocorticoid receptor (GR) alpha, but not GRbeta in mood disorder patients, suggesting an aberrant alternative splicing mechanism. To examine whether altered RNA splicing may underlie the pathophysiology of mood disorder, we evaluated the expression of a variety of SR protein splicing factors, a family of proteins indispensable for proper alternative splicing, in mood disorder patients.