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Objectives: As a complex, polygenic trait, brain size has likely been influenced by a range of direct and indirect selection pressures for both cognitive and non‐cognitive functions and capabilities. It has been hypothesized that hominin brain expansion was, in part, a correlated response to selection acting on aerobic capacity (Raichlen & Polk, 2013). According to this hypothesis, selection for aerobic capacity increased the activity of various signaling molecules, including those involved in brain growth. One key molecule is brain‐derived neurotrophic factor (BDNF), a protein that regulates neuronal development, survival, and plasticity in mammals. This review updates, partially tests, and expands Raichlen and Polk's (2013) hypothesis by evaluating evidence for BDNF as a mediator of brain size. Discussion: We contend that selection for endurance capabilities in a hot climate favored changes to muscle composition, mitochondrial dynamics and increased energy budget through pathways involving regulation of PGC‐1α and MEF2 genes, both of which promote BDNF activity. In addition, the evolution of hairlessness and the skin's thermoregulatory response provide other molecular pathways that promote both BDNF activity and neurotransmitter synthesis. We discuss how these pathways contributed to the evolution of brain size and function in human evolution and propose avenues for future research. Our results support Raichlen and Polk's contention that selection for non‐cognitive functions has direct mechanistic linkages to the evolution of brain size in hominins. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Educational Practice & Research is the property of National Taipei University of Education and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Contemporary Journal of African Studies is the property of Institute of African Studies and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Autism spectrum disorders (ASDs) are neurodevelopmental disorders that share behavioral features, the results of numerous studies have suggested that the underlying causes of ASDs are multifactorial. Behavioral and/or neurobiological analyses of ASDs have been performed extensively using a valid model of prenatal exposure to valproic acid (VPA). Abnormal synapse formation resulting from altered neurite outgrowth in neural progenitor cells (NPCs) during embryonic brain development has been observed in both the VPA model and ASD subjects. Although several mechanisms have been suggested, the actual mechanism underlying enhanced neurite outgrowth remains unclear. In this study, we found that VPA enhanced the expression of brain-derived neurotrophic factor (BDNF), particularly mature BDNF (mBDNF), through dual mechanisms. VPA increased the mRNA and protein expression of BDNF by suppressing the nuclear expression of methyl-CpG-binding protein 2 (MeCP2), which is a transcriptional repressor of BDNF. In addition, VPA promoted the expression and activity of the tissue plasminogen activator (tPA), which induces BDNF maturation through proteolytic cleavage. Trichostatin A and sodium butyrate also enhanced tPA activity, but tPA activity was not induced by valpromide, which is a VPA analog that does not induce histone acetylation, indicating that histone acetylation activity was required for tPA regulation. VPA-mediated regulation of BDNF, MeCP2, and tPA was not observed in astrocytes or neurons. Therefore, these results suggested that VPA-induced mBDNF upregulation was associated with the dysregulation of MeCP2 and tPA in developing cortical NPCs. [ABSTRACT FROM AUTHOR]

Currently, the diagnosis of major depressive disorder (MDD) mainly relies on clinical examination and subjective evaluation of depressive symptoms. There is no non-invasive, quantitative test available today for the diagnosis of MDD. In MDD, exploration of biomarkers will be helpful in diagnosing the disorder as well as in choosing a treatment, and predicting the treatment response. In this article, it is aimed to review the findings of suggested biomarkers such as growth factors, cytokines and other inflammatory markers, oxidative stress markers, endocrine markers, energy balance hormones, genetic and epigenetic features, and neuroimaging in MDD and to evaluate how these findings contribute to the pathophysiology of MDD, the prediction of treatment response, severity of the disorder, and identification of subtypes. Among these, the findings related to the brain-derived neurotrophic factor, the hypothalamo-pituitary-adrenal axis, cytokines, and neuroimaging may be strong candidates for being biomarkers MDD, and may provide critical information in understanding biological etiology of depression. Although the findings are not sufficient yet, we think that the results of epigenetic studies will also provide very important contributions to the biomarker research in MDD. The availability of biomarkers in MDD will be an advancement that will facilitate the diagnosis of the disorder, treatment choices in the early stages, and prediction of the course of the disorder. [ABSTRACT FROM AUTHOR]

Purpose: The purpose of this paper is to review the impact of the clinical leadership programme, in enabling the Darzi fellows to lead change projects in health and care services, and to secure quality healthcare in the NHS beyond the lifetime of the programme.Design/methodology/approach: A longitudinal empirical investigation of clinical leaders ( n=80) over an eight-year period was framed through an activity theory (AT)-driven research methodology using a mixed-methods approach.Findings: AT illuminated how change was sustained in the NHS in London through the Darzi Clinical Leadership Fellowship. By any reasonable measurement, this programme excels, with learning and positive behavioural change sustained after the Fellowship across the NHS. Further recognition is needed of the continuing development needs of fellows as they take on more responsible leadership roles in their careers.Research Limitations/implications: Darzi fellows are a hard-to-reach group. The sample represents a response rate of 34 per cent. In total, 77 per cent of respondents emanated from cohorts 5 to 8 programmes.Practical Implications: The investment in a clinical leadership programme focused on systems leadership for quality generates value for the NHS.Social Implications: Countless interventions flowed through London's healthcare community and beyond as a result of the Fellowship. This research exposed how Darzi fellows continue to lead innovation for alternative healthcare outcomes. Many proactive fellows employ a suite of learned skills and capabilities to lead systemic change.Originality/value: This research is the first known longitudinal clinical leadership development study undertaken. The Darzi programme has created a unique clinical network of mutually supportive, team-centric systems thinkers and doers, with an evidence-based approach to systems change. Many fellows are catalysing sustainable change in the healthcare environment. [ABSTRACT FROM AUTHOR]

Background: A reliable biomarker signature for bipolar disorder sensitive to illness phase would be of considerable clinical benefit. Among circulating blood-derived markers there has been a significant amount of research into inflammatory markers, neurotrophins and oxidative stress markers.AimsTo synthesise and interpret existing evidence of inflammatory markers, neurotrophins and oxidative stress markers in bipolar disorder focusing on the mood phase of illness.Method: Following PRISMA (Preferred Reporting Items for Systematic reviews and Meta-analyses) guidelines, a systematic review was conducted for studies investigating peripheral biomarkers in bipolar disorder compared with healthy controls. We searched Medline, Embase, PsycINFO, SciELO and Web of Science, and separated studies by bipolar mood phase (mania, depression and euthymia). Extracted data on each biomarker in separate mood phases were synthesised using random-effects model meta-analyses.Results: In total, 53 studies were included, comprising 2467 cases and 2360 controls. Fourteen biomarkers were identified from meta-analyses of three or more studies. No biomarker differentiated mood phase in bipolar disorder individually. Biomarker meta-analyses suggest a combination of high-sensitivity C-reactive protein/interleukin-6, brain derived neurotrophic factor/tumour necrosis factor (TNF)-α and soluble TNF-α receptor 1 can differentiate specific mood phase in bipolar disorder. Several other biomarkers of interest were identified.Conclusions: Combining biomarker results could differentiate individuals with bipolar disorder from healthy controls and indicate a specific mood-phase signature. Future research should seek to test these combinations of biomarkers in longitudinal studies.Declaration of interestNone. [ABSTRACT FROM AUTHOR]

Aims: The aim of the study is to assess and compare serum C-reactive protein (CRP), brain derived neurotrophic factor (BDNF), and interleukin-2 (IL-2) levels in patients with first-episode depression (FED), recurrent depressive disorder (RDD), and healthy controls (HCs) and to determine the relationship between the above-specified inflammatory markers, severity of depression, and stressful life events. Materials and Methods: Consecutive drug-naive patients with FED and RDD (n = 85) and 50 HCs were studied. Serum concentrations of CRP, brain-derived nerve growth factor (BDNF), and IL-2 were measured. All participants were assessed using Mini-International Neuropsychiatric Interview Plus, Beck's depression inventory, and presumptive stressful life events scale. Results: The FED and RDD groups had statistically significant lower serum concentration of BDNF and higher IL-2 compared to the HC group, whereas no statistically significant difference was observed with regard to CRP level. No statistically significant differences were observed with regard to the severity of depression and serum concentrations of CRP, BDNF, and IL-2 in the FED and RDD groups. No significant correlation was found between severity of depression and serum concentration of CRP, BDNF, and IL-2 in both the groups. Serum CRP concentration was significantly higher in patients with ≥2 stressful life events. No significant difference was observed between number of stressful life events and BDNF and IL-2 in patients with depression. Conclusion: FED and RDD are associated with lower serum concentration of BDNF and higher IL-2 compared to the HCs, whereas there appears no difference with regard to CRP level. Multicentric studies are needed to further elucidate the role of inflammatory markers in depression. [ABSTRACT FROM AUTHOR]

Nutritional support is seen as a vital component in the battle to attenuate the extreme hypermetabolic response experienced by patients suffering from large thermal injuries. Protein catabolism precipitating protein malnutrition places patients at greater risk of wound infection and sepsis due to delayed wound healing. Underfeeding, aggressive feeding, feeding routes, timing of initiation of feeding and tight insulin control have all been explored extensively in the quest to understand what nutritional treatment will best attenuate the hypermetabolic response. Despite this it is suggested that the majority of patients with large thermal injuries do not receive adequate nutritional support immediately post injury. Nurses have a pivotal role to play in ensuring that thermal injury patients receive appropriate nutritional support based on the best available evidence. [ABSTRACT FROM AUTHOR]

Transdisciplinary approaches (TDA) have provided a useful way to assess, formulate and monitor personalized individual strategies which share a common starting point where expertise from different disciplines come together in better and more efficiently understanding the individual's special needs and their autism. This paper aims to present through a single-case study how shared formulation informing interventions and strategies have been applied by adopting a transdisciplinary embedded approach through the adoption of a model of well-being - PERMA model. Differences between multi-disciplinary and transdisciplinary approaches are briefly discussed. Identification of barriers to accessing learning, evidence-based challenging behaviour profiles, identification of sensory and functional communication needs, a shared understanding of the individual and a consistent resilient team approach are presented and discussed. Qualitative and quantitative outcomes are ultimately presented and discussed with further reflections on the impact for the wider education practice and provision. [ABSTRACT FROM AUTHOR]

Copyright of Chung Cheng Educational Studies is the property of Chung Cheng University, College of Education and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Child maltreatment (CM) and attachment experiences are closely linked to alterations in the human oxytocin (OXT) system. However, human data about oxytocin receptor (OXTR) protein levels are lacking. Therefore, we investigated oxytocin receptor (OXTR) protein levels in circulating immune cells and related them to circulating levels of OXT in peripheral blood. We hypothesized reduced OXTR protein levels, associated with both, experiences of CM and an insecure attachment representation. Methods: OXTR protein expressions were analyzed by western blot analyses in peripheral blood mononuclear cells (PBMC) and plasma OXT levels were determined by radioimmunoassay (RIA) in 49 mothers. We used the Childhood Trauma Questionnaire (CTQ) to assess adverse childhood experiences. Attachment representations (secure vs. insecure) were classified using the Adult Attachment Projective Picture System (AAP) and levels of anxiety and depression were assessed with the German version of the Hospital Depression and Anxiety scale (HADS-D). Results: CM-affected women showed significantly lower OXTR protein expression with significantly negative correlations between the OXTR protein expression and the CTQ sum score, whereas plasma OXT levels showed no significant differences in association with CM. Lower OXTR protein expression in PBMC were particularly pronounced in the group of insecurely attached mothers compared to the securely attached group. Anxiety levels were significantly higher in CM-affected women. Conclusion: This study demonstrated a significant association between CM and an alteration of OXTR protein expression in human blood cells as a sign for chronic, long-lasting alterations in this attachment-related neurobiological system. [ABSTRACT FROM AUTHOR]

Objectives: Older adults with chronic schizophrenia are at greater risk for functional disability and poorer health outcomes than those without serious mental illness. These individuals comprise 1–2% of the elderly population in the United States and are projected to number approximately 15 million by 2030. The symptoms of schizophrenia can be disabling for individuals, significantly reducing quality of life. Often, the negative symptoms (NS) are the most resistant to treatment and are considered a marker of illness severity, though they are challenging to measure objectively. Biomarkers can serve as objective indicators of health status. Brain-derived neurotrophic factor (BDNF) is a potential biomarker for schizophrenia and may serve as an important indicator of illness severity. Methods: A cross-sectional study with 30 older adults with chronic schizophrenia. Participants were assessed on serum levels of BDNF and psychiatric symptoms (Positive and Negative Syndrome Scale). Pearson’s bivariate correlations (two-tailed) and linear regression models were used. Results: A significant positive association (p < .05) was found between higher serum levels of BDNF and greater severity for the NS items of passive, apathetic, social withdrawal, and emotional withdrawal. In multivariate analyses, the association remained significant. Conclusions: Although the association between BDNF and NS was not in the expected direction, the data corroborate findings from previous work in patients with schizophrenia. It is possible that higher serum levels of BDNF reflect compensatory neuronal mechanisms resulting from neurodevelopmental dysfunction. [ABSTRACT FROM AUTHOR]

Aims: Despite the involvement of the brain-derived neurotrophic factor (BDNF) in the physiopathology of major depressive disorder (MDD), the coherence between the components of the BDNF pathway and their link with the clinical features of MDD are insufficiently studied. We aimed to assess in Caucasian depressed patients the impact of the BDNF Val66Met polymorphism on plasma BDNF levels taking into account the clinical characteristics of MDD. Methods: A total of 328 Caucasian adult MDD patients with a current major depressive episode (MDE) were assessed for the BDNF Val- 66Met polymorphism, plasma BDNF levels and clinical characteristics of the MDD. Results: Plasma BDNF levels were linearly associated with the BDNF Val66Met genotypes (ValVal: 1,525.9 ± 1,183.3 pg/mL vs. ValMet: 1,248.7 ± 1,081.8 vs. MetMet: 1,004.9 ± 952.8; p = 0.04), Met carriers having lower BDNF levels than ValVal ones. Significant interactions between the Val66Met polymorphism and 3 clinical characteristics - age at onset (p = 0.03), MDD duration (p = 0.04), and number of previous MDE (p = 0.04) - were evidenced for plasma BDNF levels. Indeed, in Met carriers, but not in ValVal ones, plasma BDNF levels were negatively correlated with age at onset and positively correlated with MDD duration and number of previous MDE. Conclusion: Our results show a measurable, coherent, and functional BDNF pathway based on the BDNF Val66Met polymorphism and plasma BDNF levels in patients with a current MDE. This pathway is related to the clinical course of major depression, plasma BDNF levels being associated with the long-term history of MDD in Met carriers. Further studies assessing central BDNF are needed to understand the underlying mechanisms of this association. [ABSTRACT FROM AUTHOR]

Electroconvulsive therapy (ECT) is an effective treatment for depression, but can have negative side effects including amnesia. The mechanisms of action underlying both the antidepressant and side effects of ECT are not well understood. An equivalent manipulation that is conducted in experimental animals is electroconvulsive seizure (ECS). Rodent studies have provided valuable insights into potential mechanisms underlying the antidepressant and side effects of ECT. However, relatively few studies have investigated the effects of ECS in animal models with a depression-relevant manipulation such as chronic stress. In the present study, mice were first exposed to chronic social stress (CSS) or a control procedure for 15 days followed by ECS or a sham procedure for 10 days. Behavioral effects were investigated using an auditory fear conditioning (learning) and expression (memory) test and a treadmill-running fatigue test. Thereafter, immunohistochemistry was conducted on brain material using the microglial marker Iba-1 and the cholinergic fibre marker ChAT. CSS did not increase fear learning and memory in the present experimental design; in both the control and CSS mice ECS reduced fear learning and fear memory expression. CSS induced the expected fatigue-like effect in the treadmill-running test; ECS induced increased fatigue in CSS and control mice. In CSS and control mice ECS induced inflammation in hippocampus in terms of increased expression of Iba-1 in radiatum of CA1 and CA3. CSS and ECS both reduced acetylcholine function in hippocampus as indicated by decreased expression of ChAT in several hippocampal sub-regions. Therefore, CSS increased fatigue and reduced hippocampal ChAT activity and, rather than reversing these effects, a repeated ECS regimen resulted in impaired fear learning-memory, increased fatigue, increased hippocampal Iba-1 expression, and decreased hippocampal ChAT expression. As such, the current model does not provide insights into the mechanism of ECT antidepressant function but does provide evidence for pathophysiological mechanisms that might contribute to important ECT side-effects. [ABSTRACT FROM AUTHOR]

Previous reports have suggested that physical and psychological stresses may trigger fibromyalgia (FM). Stress is an important risk factor in the development of depression and memory impairments. Antidepressants have been used to prevent stress-induced abnormal pain sensation. Among various antidepressants, tianeptine has been reported to be able to prevent neurodegeneration due to chronic stress and reverse decreases in hippocampal volume. To assess the possible effect of tianeptine on FM symptoms, we constructed a FM animal model induced by restraint stress with intermittent cold stress. All mice underwent nociceptive assays using electronic von Frey anesthesiometer and Hargreaves equipment. To assess the relationship between tianeptine and expression levels of brain-derived neurotrophic factor (BDNF), cAMP response element-binding protein (CREB), and phosphorylated cAMP response element-binding protein (p-CREB), western blotting and immunohistochemistry analyses were performed. In behavioral analysis, nociception tests showed that pain threshold was significantly decreased in the FM group compared to that in the control group. Western blot and immunohistochemical analyses of medial prefrontal cortex (mPFC) and hippocampus showed downregulation of BDNF and p-CREB proteins in the FM group compared to the control group. However, tianeptine recovered these changes in behavioral tests and protein level. Therefore, this FM animal model might be useful for investigating mechanisms linking BDNFCREB pathway and pain. Our results suggest that tianeptine might potentially have therapeutic efficacy for FM. [ABSTRACT FROM AUTHOR]

Background: Brain-derived neurotrophic factors are known to be related to the psychopathology of major depressive disorder. However, studies focusing on drug-naïve first-episode patients are still rare. Methods: Over a 6-year period, we examined the serum brain-derived neurotrophic factors levels in patients with first-episode drug-naïve major depressive disorder and compared them with sex-matched healthy controls. We also investigated the relationships between serum brain-derived neurotrophic factors levels, suicidal behavior, and Hamilton Depression Rating Scale scores before and after a 4-week antidepressant treatment. Results: The baseline serum brain-derived neurotrophic factors levels of 71 patients were significantly lower than those of the controls (P = .017), and the Hamilton Depression Rating Scale scores in 71 patients did not correlate with brain-derived neurotrophic factor levels. Brain-derived neurotrophic factor levels were significantly lower in 13 suicidal major depressive disorder patients than in 58 nonsuicidal major depressive disorder patients (P = .038). Among 41 followed-up patients, there was no alteration in serum brain-derived neurotrophic factors levels after treatment with antidepressants (P = .126). In receiver operating characteristic curve analysis of using pretreatment brain-derived neurotrophic factors to estimate the response to treatment, the area under the curve was 0.684. The most suitable cut-off point was 6.1 ng/mL (sensitivity = 78.6%, specificity = 53.8%). Conclusions: Our data support the serum brain-derived neurotrophic factor levels in patients with drug-naïve first-episode major depressive disorder were lower than those in the healthy controls, and patients with pretreatment brain-derived neurotrophic factors >6.1 ng/mL were more likely to be responders. Although the relationship of our results to the mechanism of drug action and pathophysiology of depression remains unclear, the measure may have potential use as a predictor of response to treatment. In the future, it needs a large sample to prove these results. [ABSTRACT FROM AUTHOR]

The measurement of circulating levels of brain-derived neurotrophic factor (BDNF) has been proposed to be a marker of disease and an indicator of recovery. Thus, knowing the temporal pattern and influence of potential circadian rhythms is important. Although several studies have measured BDNF at different times of day, no studies have done so while controlling for potential masking influences such as sleep and activity. Further, no previous study has examined circadian rhythms within individuals. We examined circadian rhythms in plasma BDNF while minimizing masking from behavioral and environmental factors using a 30-h constant routine (CR) protocol. In a sample of 39 healthy adults, we found significant circadian rhythms in 75% of women and 52% of men. The timing of the acrophase of the BDNF rhythm, however, was unrelated to clock time in women, while it was related to clock time in men. These results indicate that the use of single-sample measures of plasma BDNF as a marker of disease will be unreliable, especially in women. Repeated plasma BDNF samples over a 24-h period within individuals would be needed to reveal abnormalities related to disease states. [ABSTRACT FROM AUTHOR]

In the last 10 years sport psychology expanded its applicability in a variety of fields which have helped to address some of the challenges related to high level performance and sport competition. When we talk about performance in its wider sense, sport psychology is able to help develop a better understanding on how strategies can be adopted in improving general human performance levels. This includes increasing the knowledge of key concepts such as motivation, self-confidence and resilience. Furthermore performance in its wider sense helps in the understanding of the impact of stress and arousal and how these can affect both positively and negatively performance levels including appreciating individual differences as well as dynamics between groups of individuals. In this paper performance rather than solely be related to the field of competitive or professional sport has been discussed in people with ASCs and aims to explore how by adopting a positive psychological model in the formulation of individual assessments and subsequent interventions have led to improvement in individual skills, participation, engagement and ultimately quality of life. Positive psychological principles, such as the role of wellbeing and wellness, the PERMA Model has increased our understanding of human potentials, performance and wellbeing. The aim of this paper is to present and reflect on the applicability and benefits of adopting sport psychology models, the PERMA model and positive psychological principles in special education and care settings with the presentation and discussion of their theoretical and some practical implementation in two case studies. [ABSTRACT FROM AUTHOR]

Background: Various antidepressants occupy brain serotonin transporter (SERT), decrease platelet serotonin (5-HT) concentration, and normalize reduced plasma brain-derived neurotrophic factor (BDNF) concentrations in depressed patients. Vortioxetine is a recently introduced antidepressant with a multimodal mechanism of action. In addition to SERT inhibition, vortioxetine acts via different 5-HT receptors. To further elucidate its mechanism of action, we have investigated the effects of vortioxetine on platelet 5-HT and plasma BDNF concentrations in patients with major depression. Methods: Platelet 5-HT and plasma BDNF concentrations were determined in 44 healthy subjects at baseline and in 44 depressed patients before and after 4 weeks of treatment with vortioxetine (5-15 mg daily). Platelet 5-HT concentration was determined using the ortho-phthalaldehyde-enhanced fluorometric method, and plasma BDNF concentration using a commercial enzyme-linked immunosorbent assay (Quantikine ELISA, R&D Systems). Results: At baseline, platelet 5-HT concentrations did not differ between depressed and control subjects, but plasma BDNF values were lower ( p = 0.011; ω = 0.80) in depressed patients than in healthy subjects. Vortioxetine treatment significantly ( p < 0.0001; ω = 0.80) decreased platelet 5-HT concentration and significantly ( p = 0.004; ω = 0.80) increased plasma BDNF concentration in depressed patients compared to their baseline values. Age, gender, and smoking were not significantly associated with platelet 5-HT and plasma BDNF concentrations. Conclusion: Despite a novel mechanism of action, vortioxetine shares some common effects with other antidepressants. This study is the first to show that, in addition to clinical improvement, 4 weeks of treatment with vortioxetine (5-15 mg daily), decreased platelet 5-HT and increased plasma BDNF concentrations in depressed patients. [ABSTRACT FROM AUTHOR]

Objective: To explore associations of the brain-derived neurotrophic factor (BDNF) Val66Met polymorphism with cognitive functioning and psychopathology in patients with schizophrenia. Methods: We included 133 subjects meeting the DSM-IV criteria for schizophrenia who were in the post-acute stage of the disease. BDNF Val66Met genotypes were identified via polymerase chain reaction. The computerized neurocognitive function battery, Positive and Negative Syndrome Scale (PANSS), Calgary Depression Scale for Schizophrenia (CDSS), Social and Occupational Functioning Scale (SOFAS), and the Subjective Well-being under Neuroleptic Treatment (SWN-K) were administered. Gender-stratified sub-analysis was also conducted to identify gender-specific patterns in the findings. Results: In male patients, no significant difference in any measure by BDNF genotype was evident. In female patients, scores on the CDSS and total PANSS and all subscales were significantly higher in valine (Val) carriers. In addition, scores on the SOFAS and SWN-K were significantly lower in Val carriers. In terms of neurocognitive measures, female patients with the Val allele had significantly poorer reaction times and fewer correct responses on the Continuous Performance Test (CPT) and the Trail Making Test (Parts A and B). After adjustment of PANSS total scores and log-transformed CDSS scores, CPT outcomes were significantly poorer in female patients with than in those without the Val allele. Conclusion: Gender-specific associations of the Val allele with poor neurocognitive function and more severe psychopathology were evident. Further studies are required to explore the mechanisms of these differences and the potential utility of the BDNF genotype as a predictor of outcome in patients with schizophrenia. [ABSTRACT FROM AUTHOR]

Copyright of Cultura Neolatina is the property of Mucchi Editore and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background and aims: Gambling disorder (GD) shares many similarities with substance use disorders (SUDs) in clinical, neurobiological, and neurocognitive features, including decision-making. We evaluated the relationships among, GD, decision-making, and brain-derived neurotrophic factor (BDNF), as measured by serum BDNF levels. Methods: Twenty-one male patients with GD and 21 healthy sex- and age-matched control subjects were evaluated for associations between serum BDNF levels and the Problem Gambling Severity Index (PGSI), as well as between serum BDNF levels and Iowa Gambling Task (IGT) indices. Results: The mean serum BDNF levels were significantly increased in patients with GD compared to healthy controls. A significant correlation between serum BDNF levels and PGSI scores was found when controlling for age, depression, and duration of GD. A significant negative correlation was obtained between serum BDNF levels and IGT improvement scores. Discussion: These findings support the hypothesis that serum BDNF levels constitute a dual biomarker for the neuroendocrine changes and the severity of GD in patients. Serum BDNF level may serve as an indicator of poor decision-making performance and learning processes in GD and help to identify the common physiological underpinnings between GD and SUDs. [ABSTRACT FROM AUTHOR]

Suicidality is a continuum ranging from ideation to attempted and completed suicide, with a complex etiology involving both genetic heritability and environmental factors. The majority of suicide events occur in the context of psychiatric conditions, preeminently major depression and bipolar disorder. The present study investigates clinical factors associated with suicide in a sample of 553 mood disorder patients, recruited within the 'Psy Pluriel' center, Centre Européen de Psychologie Médicale, and the Department of Psychiatry of Erasme Hospital (Brussels). Furthermore, genetic association analyses examining polymorphisms within COMT, BDNF, MAPK1 and CREB1 genes were performed in a subsample of 259 bipolar patients. The presence or absence of a previous suicide attempt and of current suicide risk were assessed. A positive association with suicide attempt was reported for younger patients, females, lower educated, smokers, those with higher scores on depressive symptoms and higher functional disability and those with anxiety comorbidity and familial history of suicidality in first- and second-degree relatives. Anxiety disorder comorbidity was the stronger predictor of current suicide risk. No associations were found with polymorphisms within COMT and BDNF genes, whereas significant associations were found with variations in rs13515 (MAPK1) and rs6740584 (CREB1) polymorphisms. From a clinical perspective, our study proposes several clinical characteristics, such as increased depressive symptomatology, anxiety comorbidity, functional disability and family history of suicidality, as correlates associated with suicide. Genetic risk variants in MAPK1 and CREB1 genes might be involved in a dysregulation of inflammatory and neuroplasticity pathways and are worthy of future investigation. [ABSTRACT FROM AUTHOR]

There is a dearth of evidence from non-Western populations and contexts in the sport psychology literature. With increasing attention given to the development of cultural sport psychology and decentralizing sport psychology evidence, this is the first study to document the effectiveness of applied interventions in non-Western populations (herein, India). With a rigorous methodological design, we randomly distributed a sample of 90 adolescents into three skill groups (discrete, serial, and continuous) and separated them across the team and individual sports. A random assignment of participants to two experimental groups, that is, imagery and video modeling interventions, and a control group was conducted for the duration of a 66-day intervention. Sport psychology imagery and video modeling interventions were provided in addition to skills training across all groups. Repeated-measures analyses of variance demonstrated that the intervention groups exhibited positive outcomes on skill execution (across discrete, serial, and continuous skills) and anxiety compared with the control group (p <.05). The findings of this study provide novel evidence that video modeling and imagery interventions are effective among a non-Western adolescent population. The context of this high-impact intervention case study, the intervention, and the challenges of developing and delivering the intervention are discussed along with their practical significance for future research and applied practice. [ABSTRACT FROM AUTHOR]

In these last decades, emotions and feelings, neglected for centuries by experimental sciences, have become the topic of extensive neuroscientific research. Currently, love, the most typically human feeling, can be viewed as the result of different phases (steps), each regulated by evolutionary well-conserved and integrated neural substrates. We have proposed that the early stage, generally called romantic love, is the result of the activation of the brain limbic structures regulating fear/anxiety reactions leading to changes of major neurotransmitters, such as increased monoamine levels and decreased serotonin concentrations. The second stage of love is mainly underlain by the structures regulating the attachment system and involving oxytocin and vasopressin neuropeptides and neurotrophins. This would explain why the positive effects of love can be extremely beneficial for both mental and physical health.However, available data are still limited, and the proposed models, although supported by converging data, should be considered speculative and oversimplified. The hope is that neuroscience will permit to shed light on love, one of the most intriguing, and still largely unknown mysteries of human nature., (© 2021. The Author(s), under exclusive license to Springer Nature Switzerland AG.)

Background: The predictive therapeutic value of brain derived neurotrophic factor (BDNF) and its changes associated with the use of specific antidepressants are still unclear. In this study, we examined BDNF as a peripheral and NAA as a central biomarker over the time course of antidepressant treatment to specify both of their roles in the response to the medication and clinical outcome. Methods: We examined serum BDNF (ELISA kit) in a sample of 76 (47 female and 29 male) depressed patients in a naturalistic setting. BDNF was assessed before medication and subsequently after two, four and six weeks of antidepressant treatment. Additionally, in fifteen patients, N-acetylaspartate (NAA) was measured in the anterior cingulate cortex (ACC) with magnetic resonance spectroscopy (MRS). Over a time course of six weeks BDNF and NAA were also examined in a group of 41 healthy controls. Results: We found significant lower serum BDNF concentrations in depressed patients compared to the sample of healthy volunteers before and after medication. BDNF and clinical symptoms decreased significantly in the patients over the time course of antidepressant treatment. Serum BDNF levels at baseline predicted the symptom outcome after eight weeks. Specifically, responders and remitters had lower serum BDNF at baseline than the nonresponders and nonremitters. NAA was slightly decreased but not significantly lower in depressed patients when compared with healthy controls. During treatment period, NAA showed a tendency to increase. Limitations: A relative high drop-out rate and possibly, a suboptimal observation period for BDNF. Conclusion: Our data confirm serum BDNF as a biomarker of depression with a possible role in response prediction. However, our findings argue against serum BDNF increase being a prerequisite to depressive symptom reduction. [ABSTRACT FROM AUTHOR]

Background: Long-term neuroimmune activation is a common finding in major depressive disorder (MDD). Literature suggests a dual effect of electroconvulsive therapy (ECT), a highly effective treatment strategy for MDD, on neuroimmune parameters: while ECT acutely increases inflammatory parameters, such as serum levels of pro-inflammatory cytokines, there is evidence to suggest that repeated ECT sessions eventually result in downregulation of the inflammatory response. We hypothesized that this might be due to ECT-induced attenuation of microglial activity upon inflammatory stimuli in the brain.Methods: Adult male C57Bl/6J mice received a series of ten electroconvulsive seizures (ECS) or sham shocks, followed by an intracerebroventricular (i.c.v.) lipopolysaccharide (LPS) or phosphate-buffered saline (PBS) injection. Brains were extracted and immunohistochemically stained for the microglial marker ionized calcium-binding adaptor molecule 1 (Iba1). In addition, a sucrose preference test and an open-field test were performed to quantify behavioral alterations.Results: LPS induced a short-term reduction in sucrose preference, which normalized within 3 days. In addition, LPS reduced the distance walked in the open field and induced alterations in grooming and rearing behavior. ECS did not affect any of these parameters. Phenotypical analysis of microglia demonstrated an LPS-induced increase in microglial activity ranging from 84 to 213 % in different hippocampal regions (CA3 213 %; CA1 84 %; dentate gyrus 131 %; and hilus 123 %). ECS-induced alterations in microglial activity were insignificant, ranging from -2.6 to 14.3 % in PBS-injected mice and from -20.2 to 6.6 % in LPS-injected mice.Conclusions: We were unable to demonstrate an effect of ECS on LPS-induced microglial activity or behavioral alterations. [ABSTRACT FROM AUTHOR]

Emerging data suggest that Electro-Convulsive Treatment (ECT) may reduce depressive symptoms by increasing the expression of Brain-Derived Neurotrophic Factor (BDNF). Yet, conflicting findings have been reported. For this reason we performed a systematic review and meta-analysis of the preclinical and clinical literature on the association between ECT treatment (ECS in animals) and changes in BDNF concentrations and their effect on behavior. In addition, regional brain expression of BDNF in mouse and human brains were compared using Allen Brain Atlas. ECS, over sham, increased BDNF mRNA and protein in animal brain (effect size [Hedge’s g]: 0.38―0.54; 258 effect-size estimates, N = 4,284) but not in serum (g = 0.06, 95% CI = -0.05―0.17). In humans, plasma but not serum BDNF increased following ECT (g = 0.72 vs. g = 0.14; 23 effect sizes, n = 281). The gradient of the BDNF increment in animal brains corresponded to the gradient of the BDNF gene expression according to the Allen brain atlas. Effect-size estimates were larger following more ECT sessions in animals (r = 0.37, P < .0001) and in humans (r = 0.55; P = 0.05). There were some indications that the increase in BDNF expression was associated with behavioral changes in rodents, but not in humans. We conclude that ECS in rodents and ECT in humans increase BDNF concentrations but this is not consistently associated with changes in behavior. [ABSTRACT FROM AUTHOR]

This paper reports findings about parents' experiences of caring for young people with Autistic Spectrum Conditions (ASCs) moving into adulthood. In‐depth interviews were conducted with 38 parents of young people (15–21 years) with ASCs. Data were analysed thematically. In the perceived absence of service support, parents' acted as ‘care‐coordinators’ and ‘life‐supporters’ for their child as they moved into adulthood. These roles came with little choice, emotional demands and personal restrictions. Being supported was important for parents, but preferences differed regarding what this should look like. Implications for policy are discussed. [ABSTRACT FROM AUTHOR]

Data is inconsistent concerning the question whether cognitive-physical training (CPT) yields stronger cognitive gains than cognitive training (CT). Effects of additional counseling, neurobiological mechanisms, and predictors have scarcely been studied. Healthy older adults were trained with CT (n = 20), CPT (n = 25), or CPT with counseling (CPT+C; n = 23). Cognition, physical fitness, BDNF, IGF-1, and VEGF were assessed at pre- and post-test. No interaction effects were found except for one effect showing that CPT+C led to stronger gains in verbal fluency than CPT (p = 0.03). However, this superiority could not be assigned to additional physical training gains. Low baseline cognitive performance and BDNF, not carrying apoE4, gains in physical fitness and the moderation of gains in physical fitness × gains in BDNF predicted training success. Although all types of interventions seem successful to enhance cognition, our data do not support the hypotheses that CPT shows superior CT gains compared to CT or that CPT+C adds merit to CPT. However, as CPT leads to additional gains in physical fitness which in turn is known to have positive impact on cognition in the long-term, CPT seems more beneficial. Training success can partly be predicted by neuropsychological, neurobiological, and genetic parameters. [ABSTRACT FROM AUTHOR]

This work examined the acquisition of information about gases using a virtual sensor array and classification. We were particularly interested in the approach in which classes are defined in a qualitative–quantitative manner, that is, by identifying the gas and concentration range. This type of information will be of interest for air pollution assessment purposes. In this field of application, it is often not necessary to provide very precise information. The idea of the virtual sensor array exploits the dependence of a gas sensor’s response on operating conditions. Originally it was developed as a means to improve the selectivity of an electronic nose when energy consumption by this device was a serious limitation. If the response of one sensor is measured inntime points, and each time point is characterised by different controlled exposure conditions, the sensor becomes analogous to ann-dimensionalvirtual sensor array. Compared with conventional approaches, a virtual sensor array based on a single sensor offers low power consumption, low volume, and low cost, which opens up new markets for wide application of portable and handheld devices. In this article, we show that a virtual sensor array and classification may serve as a reliable source of qualitative–quantitative information about gases. Twenty-six classes (five substances, each at five concentration ranges, and pure air) were recognised with a true positive rate higher than 99.14 ± 0.49% and a true negative rate higher than 99.21 ± 0.52%. As demonstrated, the basis for recognition could be a virtual sensor array associated with a low-power consuming sensor (210–280 mW). The complexity of the applied classifier could be adjusted depending on the choice of sensor operating conditions. For a complex classifier like support vector machine, dynamic exposure was sufficient to obtain high classification performance. A simpler classifier likek-nearest neighbours required more information, that is, information associated with static as well as dynamic exposure. [ABSTRACT FROM PUBLISHER]

Brain-derived neurotrophic factor ( BDNF) serves as a vital regulator of neuronal proliferation and survival, and has been shown to regulate energy homeostasis, glucose metabolism and body weight maintenance. Elevated concentrations of plasma BDNF have been associated with obesity and type 2 diabetes mellitus. Acute aerobic exercise transiently increases circulating BDNF, potentially correcting obesity-related metabolic impairment. The present study aimed to compare acute aerobic exercise elicited BDNF responses in obese and normal-weight subjects. Furthermore, we aimed to investigate whether acute exercise-induced plasma BDNF elevations would be associated with improved indices of insulin resistance, as well as substrate utilization [carbohydrate oxidation ( CHOoxi) and fat oxidation ( FAToxi)]. Twenty-two healthy, untrained subjects [11 obese (four men and seven women; age = 22.91 ± 4.44 years; body mass index = 35.72 ± 4.17 kg/m2) and 11 normal-weight (five men and six women; age = 23.27 ± 2.24 years; body mass index = 21.89 ± 1.63 kg/m2)] performed 30 min of continuous submaximal aerobic exercise at 75% maximal oxygen consumption. Our analyses showed that the BDNF response to acute aerobic exercise was similar in obese and normal-weight subjects across time (time: P = 0.015; group: P = not significant) and was not associated with indices of IR. Although no differences in the rates of CHOoxi and FAToxi were found between both groups, total relative energy expenditure was significantly lower in obese subjects compared to normal-weight subjects (3.53 ± 0.25 versus 5.59 ± 0.85; P < 0.001). These findings suggest that acute exercise-elicited BDNF elevation may not be sufficient to modulate indices of IR or the utilization of either carbohydrates or fats in obese individuals. [ABSTRACT FROM AUTHOR]

Though the role of brain derived neurotrophic factor (BDNF) as a marker for major depressive disorder (MDD) and antidepressant efficacy has been widely studied, the role of BDNF in distinct groups of patients remains unclear. We evaluated the diagnostic value of BDNF as a marker of disease severity measured by HAM-D scores and antidepressants efficacy among MDD patients. Fifty-one patients who met DSM-IV criteria for MDD and were prescribed antidepressants and 38 controls participated in this study. BDNF in serum was measured at baseline, 1st, 2nd and 8th treatment weeks. Depression severity was evaluated using the Hamilton Rating Scale for Depression (HAM-D). BDNF polymorphism rs6265 (val66met) was genotyped. We found a positive correlation between blood BDNF levels and severity of depression only among untreated women with severe MDD (HAM-D>24). Serum BDNF levels were lower in untreated MDD patients compared to control group. Antidepressants increased serum BDNF levels and reduced between-group differences after two weeks of treatment. No correlations were observed between BDNF polymorphism, depression severity, duration of illness, age and BDNF serum levels. Further supporting the role of BDNF in the pathology and treatment of MDD, we suggest that it should not be used as a universal biomarker for diagnosis of MDD in the general population. However, it has diagnostic value for the assessment of disease progression and treatment efficacy in individual patients. [ABSTRACT FROM AUTHOR]

The study aims to investigate the effect of repeated infusions of recombinant erythropoietin (EPO) on plasma brain derived neurotrophic factor (BDNF) levels in patients with affective disorders. In total, 83 patients were recruited: 40 currently depressed patients with treatment-resistant depression (TRD) (Hamilton Depression Rating Scale-17 items (HDRS-17) score >17) (study 1) and 43 patients with bipolar disorder (BD) in partial remission (HDRS-17 and Young Mania Rating Scale (YMRS) ≤ 14) (study 2). In both studies, patients were randomised to receive eight weekly EPO (Eprex; 40,000 IU) or saline (0.9% NaCl) infusions in a double-blind, placebo-controlled, parallel—group design. Plasma BDNF levels were measured at baseline and at weeks 5, 9 and at follow up, week 14. In contrast with our hypothesis, EPO down regulated plasma BDNF levels in patients with TRD (mean reduction at week 9 (95% CI): EPO 10.94 ng/l (4.51-21.41 ng/l); mean increase at week 9: Saline 0.52 ng/l, p=0.04 (-5.88-4.48 ng/l) p=0.04, partial ŋ2=0.12). No significant effects were found on BDNF levels in partially remitted patients with BD (p=0.35). The present effects of EPO on BDNF levels in patients with TRD point to a role of neurotrophic factors in the potential effects of EPO seen in TRD and BD. The neurobiological mechanisms underlying these effects and the interaction between EPO and peripheral levels on BDNF need to be further elucidated in human studies including a broad range of biomarkers. Trial Registration: ClinicalTrials.gov: . [ABSTRACT FROM AUTHOR]

Electroconvulsive therapy (ECT) is a well-established, safe and effective treatment in severest or drug-resistant affective disorders. The potential relation between any peripheral biological marker and the seizure quality as a surrogate for treatment efficacy has not been investigated so far. We prospectively examined serum brain-derived neurotrophic factor (BDNF) levels in 20 patients with major depression before and after electroconvulsive therapy. A seizure quality sum score for every ECT session was build up on the basis of the seizure duration, seizure amplitude, central inhibition, interhemispheric coherence and sympathetic activation. Serum BDNF levels were significantly higher after ECT ( P = 0.036). In the linear regression analysis, a significant correlation of the serum BDNF levels and the time between the last ECT and the blood withdrawal ( P = 0.01) was observed. The ANOVA revealed a significant influence of the interval between the last ECT and the blood withdrawal ( P = 0.0017) as well as the seizure quality ( P = 0.038) on the variance of BDNF serum levels. Our data corroborate the neurotrophin hypothesis suggesting an ECT-induced central BDNF rise leading to a delayed (>6 days) and increased equilibrium of the peripheral BDNF. The association of seizure adequacy with a BDNF rise might underline the importance of monitoring seizure quality markers in daily practice. [ABSTRACT FROM AUTHOR]

This paper explores the storylines of four student ballet dancers who attend a specialist performing arts secondary school and who, in differing ways, envisage futures which ‘look straight at ballet’. When decisions about schooling intermingle with long-held imaginings of futures in ballet, thought is provoked about ways the young adolescents embody and express notions of becoming. A Deleuzian lens is employed to explore assemblages of the self through the deterritorialisation that is provoked when unforeseen images emerge and imaginings are challenged. The data discussed in this paper include interview transcripts and pictures participants have drawn of themselves. The analysis uses notions of rhizomatic becoming and positions students' decision-making in oscillation between deterritorialisation and reterritorialisation as new languages make sense of how a future in ballet is configured from different perspectives. Themes of being in love with ballet and identities of dancers/non-dancers are negotiated through the data. As talented ballet students are compelled to move away from schooling in order to move closer to their future, concepts of schooling are problematised. Understandings of rhizomatic structures offer insight into the working out of desires, particularly in the context of a specialist performing arts school. [ABSTRACT FROM AUTHOR]

The levels of brain-derived neurotrophic factor (BDNF) are significantly decreased in patients with schizophrenia and correlate with impairments in cognitive function. However, no study has investigated the relationship between the serum BDNF levels and decision-making. We compared patients with schizophrenia to healthy controls with respect to their decision-making ability and serum BDNF levels. Eighty-six chronic schizophrenia patients and 51 healthy controls participated in this study. We controlled for gender, age, and estimated intelligence quotient (IQ), and we investigated the differences in decision-making performance on the Iowa Gambling Task (IGT) between the schizophrenia patient and control groups. We also compared the IGT scores, the serum BDNF levels, and the clinical symptoms between the groups. The IGT scores of the schizophrenia patients were lower than those of the controls. A negative correlation was detected between the mean net scores on the trials in the final two blocks and the serum BDNF levels (p < 0.05). Multiple regression analysis revealed that depressive symptoms and the serum BDNF levels were significantly associated with the mean net scores on the trials in the final two blocks. Based on these results, impaired sensitivity to both reward and punishment is associated with depressive symptoms and reduced serum BDNF levels in chronic schizophrenia patients and may be related to their poor performance on the IGT. [ABSTRACT FROM AUTHOR]

Objectives. Low serum BDNF levels have been found in depressed patients. No study has systematically investigated whether individual symptoms or symptom profiles within a depressed population contribute to low BDNF levels found in depressed subjects. Methods. All 1070 patients with a past 6-month diagnosis of major depressive disorder from the Netherlands Study of Depression and Anxiety (NESDA) were included. Composite International Diagnostic Interview (CIDI) and Inventory of Depressive Symptoms (IDS) items were tested individually in separate multiple regression analyses with serum BDNF level as the dependent and the CIDI or IDS item as independent variable. Subsequently, we compared BDNF levels between patients with seasonal affective disorder (based on the Seasonal Pattern Assessment Questionnaire) and melancholic depression, atypical depression and moderate depression (based on a latent class analysis). All analyses were adjusted for confounders. Results. Only one item was significantly associated with serum BDNF levels, namely the CIDI item 'loss of interest' (β = 0.14; P < 0.01). Counterintuitively the presence of this symptom was associated with higher BDNF levels. Other items and the comparison between different types of depression did not reveal significant differences. Conclusions. Decreased serum BDNF levels in depression cannot be attributed to a specific symptom or symptom cluster. [ABSTRACT FROM AUTHOR]

Recent studies have evaluated the role of brain-derived neurotrophic factor (BDNF) in mood disorders; however, little is known about alterations in nerve growth factor (NGF) and glial cell line-derived neurotrophic factor (GDNF). The aim of this study was to evaluate differences among serum neurotrophic factors (BDNF, NGF and GDNF) in depressed patients and healthy controls and to verify the association between serum neurotrophic levels and clinical characteristics in a young, depressed population stratified by gender. This is a cross-sectional study with depressed patients and population controls 18-29 years of age. The concentrations of neurotrophic factors were determined by the ELISA method. The diagnosis of depression and the duration of the disease were assessed by the Structured Clinical Interview according to the diagnostic and statistical manual of mental disorders. Depression severity was measured with the 17-item Hamilton Rating Scale for Depression, and the severity of anxiety symptoms was measured using the Hamilton Anxiety Rating Scale. Serum BDNF and GDNF were lower in major depressive disorder (MDD) patients compared to controls ( p ≤ 0.001). Serum NGF levels were higher in MDD patients versus controls ( p ≤ 0.001). BDNF was associated with the duration of disease only in women ( p = 0.005). GDNF was not associated with clinical characteristics in either gender. In women, NGF was associated with the severity of depressive symptoms ( p = 0.009), anxiety ( p = 0.011) and disease duration ( p = 0.005). NGF was associated with disease duration in men ( p = 0.026). Our results demonstrated that significant neurochemical differences in NGF and BDNF, but not in GDNF, were associated with the clinical features of MDD when patients were stratified by gender. [ABSTRACT FROM AUTHOR]

Objectives. To evaluate whether electroconvulsive therapy (ECT), a very effective non-pharmacological treatment for mood disorders, induces neurotrophic effects, indexed by the measurement of peripheral brain-derived neurotrophic factor (BDNF) levels. Methods. Systematic review and meta-analysis of clinical trials published in PubMed/Medline from the first date available to October 2013. We included studies measuring pre- and post-BDNF blood levels under ECT in patients with mood disorders in the acute depressive episode. Results. Eleven studies ( n = 221 subjects) were eligible. These studies enrolled subjects with unipolar, bipolar and psychotic depression and varied regarding electrode placement (unipolar vs. bipolar) and previous use of pharmacotherapy. Nonetheless, BDNF significantly increased after ECT (Hedges' g pooled, random-effects model of 0.354; 95% CI = 0.162-0.546). The results were robust according to sensitivity analysis and Begg's funnel plot did not suggest publication bias. Meta-regression results did not show association of the outcome with any clinical and demographic variable, including depression improvement. Conclusions. Our meta-analysis indicates that, similar to pharmacological interventions, peripheral BDNF increases after ECT treatment. The lack of correlation between BDNF increasing and depression improvement suggests that ECT induces neurotrophic effects regardless of clinical response in depression. [ABSTRACT FROM AUTHOR]

Remission is the primary goal of treatment for bipolar disorder I (BDI). Metabolites of noradrenaline and dopamine, 3-methoxy-4-hydroxyphenylglycol (MHPG) and homovanillic acid (HVA), respectively, are reduced by treatment with antipsychotics, but whether these phenomena are caused by antipsychotics or by the pathophysiology of BDI is not known. Interactions between brain-derived neurotrophic factor (BDNF) and mood disorders have also been suggested. We conducted a multifaceted study in BDI patients to ascertain if biological markers are associated with the manic state. Patients with Young Mania Rating Scale (YMRS) scores >20 participated in the study. Final analyses involved 24 BDI patients (13 men and 11 women). We used YMRS scores to identify mania stages in individual BDI patients (i.e., manic syndrome, response and remission stages). Statistical analyses were done using one-way repeated-measures analyses of variance (rep-ANOVA) throughout manic syndrome, response and remission stages. Plasma concentrations of MHPG and HVA were analyzed by high-performance liquid chromatography with electrochemical detection. Plasma levels of BDNF were measured by sandwich enzyme-linked immunosorbent assay. BDI patients had significantly reduced plasma levels of MHPG throughout manic syndrome, response and remission stages (rep-ANOVA, p = 0.002). Without a case of response state, there was a significant positive correlation between YMRS scores and plasma levels of MHPG (ρ = 0.33, p = 0.033, n = 48). Plasma levels of HVA and BDNF were not significantly altered throughout manic syndrome, response and remission stages. These data suggest that the peripheral level of MHPG (which is associated with noradrenaline levels in the brain) could be used as a biomarker for the manic state in BDI. The MHPG level is likely to reflect the clinical characteristics of the manic syndrome in BDI, and noradrenaline may reflect the pathophysiology from manic to remission states. [ABSTRACT FROM AUTHOR]

In the present study, we examined whether neuropsychiatric symptoms were correlated with plasma brain-derived neurotrophic factor (BDNF) levels as a state marker or were associated with the BDNF polymorphism Val66Met in patients with amnestic mild cognitive impairment (A-MCI) or Alzheimer disease (AD). One hundred and seventy-six outpatients with AD ( n = 129) or A-MCI ( n = 47) were selected and their plasma BDNF concentrations measured. Next, we investigated the correlation between the plasma BDNF level and the Behavioral Pathology in Alzheimer Disease (Behave-AD) subscale scores, which reflect neuropsychiatric symptoms. We also compared the plasma BDNF level and the Behave-AD subscale scores among the BDNF Val66Met genotypic groups. Among the seven Behave-AD subscale scores, aggressiveness was positively correlated with the plasma BDNF level ( ρ = 0.237, P < 0.005), but did not differ significantly among the three BDNF Val66Met genotypic groups. The Behave-AD total and other subscale scores did not differ significantly among the BDNF Val66Met genotypic groups and were not associated with the plasma BDNF level. Moreover, the plasma BDNF level did not differ significantly among the three BDNF Val66Met genotypic groups or between patients with A-MCI and those with AD. The plasma BDNF level was robustly correlated with aggressiveness, implying that the plasma BDNF level might be useful as a behavioral state marker in patients with AD or A-MCI. [ABSTRACT FROM AUTHOR]