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Predatory journals (PJ) exploit the open-access model promising high acceptance rate and fast track publishing without proper peer review. At minimum, PJ are eroding the credibility of the scientific literature in the health sciences as they actually boost the propagation of errors. In this article, we identify issues with PJ and provide several responses, from international and interdisciplinary perspectives in health sciences. Authors, particularly researchers with limited previous experience with international publications, need to be careful when considering potential journals for submission, due to the current existence of large numbers of PJ. Universities around the world, particularly in developing countries, might develop strategies to discourage their researchers from submitting manuscripts to PJ or serving as members of their editorial committees.

Tardive dyskinesia (TD) is a severe condition characterized by repetitive involuntary movement of orofacial regions and extremities. Patients treated with antipsychotics typically present with TD symptomatology. Here, we conducted the largest GWAS of TD to date, by meta-analyzing samples of East-Asian, European, and African American ancestry, followed by analyses of biological pathways and polygenic risk with related phenotypes. We identified a novel locus and three suggestive loci, implicating immune-related pathways. Through integrating trans-ethnic fine mapping, we identified putative credible causal variants for three of the loci. Post-hoc analysis revealed that SNPs harbored in TNFRSF1B and CALCOCO1 independently conferred three-fold increase in TD risk, beyond clinical risk factors like Age of onset and Duration of illness to schizophrenia. Further work is necessary to replicate loci that are reported in the study and evaluate the polygenic architecture underlying TD.

Neuropsychological studies have reported that attention, memory, language, motor and emotion processing are impaired in schizophrenia. It is known that schizophrenia involves structural alterations in the white matter of brain that contribute to the pathophysiology of the disorder. Uncinate fasciculus (UNC), a bundle of white matter fibres, plays an important role in the pathology of this disorder and involved in cognitive functions such as memory, language and emotion processing. Therefore, the present study aimed to investigate microstructural changes in UNC fibre in schizophrenia patients relative to controls and its correlation with neuropsychological scores. Diffusion tensor imaging (DTI) and Hindi version of Penn Computerised Neuropsychological Battery test was performed in 14 schizophrenia patients and 14 controls. DTI measures [fractional anisotropy (FA) and mean diffusivity (MD)] from UNC fibre were calculated and a comparison was made between patients and controls. Pearson’s correlation was performed between neuropsychological scores and DTI measures. Schizophrenia patients showed significantly reduced FA values in UNC fibre compared to controls. In schizophrenia patients, a positive correlation of attention, spatial memory, sensorimotor dexterity and emotion with FA was observed. These findings suggest that microstructural changes in UNC fibre may contribute to underlying dysfunction in the cognitive functions associated with schizophrenia.

Background: The functional outcome of the debilitating mental illness schizophrenia (SZ) has an integral role in cognition. The thyroid hormone has a vital role in the developmental stages and functioning of the human brain. Aim: This study aimed to evaluate the relationship between thyroid functions, cognition, and functional imaging of the brain in persons with SZ. Materials and Methods: Sixty SZ (Diagnostic and Statistical Manual (DSM-5)) persons, aged 18-50 years of both genders, were recruited in this cross-sectional observational study. Positive and Negative Syndrome Scale (PANSS) and Trail Making Tests (TMTs) A and B were administered to all patients. To assess the level of thyroid hormone, a test was conducted. Functional connectivity of the brain was assessed using resting-state functional magnetic resonance imaging (rs-fMRI). Data analysis was performed by descriptive and analytical statistical methods. FSL version 5.9 (FMRIB's) software was used for analyses of fMRI neuroimages. Results: There were no significant differences between the two populations on sociodemographic factors. The average value for thyroid-stimulating hormone (TSH) in the hypothyroid group (n = 12) and the euthyroid group (n = 47) was 8.38 mIU/l and 2.44 mIU/l, respectively. The average time in seconds for TMT-A and TMT-B was 87.27 and 218.27 in the hypothyroid group and 97.07 and 293.27 in the euthyroid group, respectively. Similarly, in the sample matched on age, gender, and age at onset of illness, there were no significant differences in demographic and clinical factors and resting-state network (RSN) between the hypothyroid (N = 10) and euthyroid (N = 10) groups. Conclusion: No differences were found in the functional brain network between the hypothyroid and euthyroid groups as the study sample did not include clinically hypothyroid persons with SZ.

Background The prevalence of mental health disorders is increasing globally. Countries in South Asia, Southeast Asia and the Middle East regions carry high burdens of mental health need; however, there are relatively few mental health research publications from this region, suggesting inadequate research funds and a paucity of qualified research personnel. To increase and strengthen the pool of mental health researchers in India and Egypt, we conducted three psychiatric research programmes in these countries: the Training Program for Psychiatric Genetics in India (2002–2011), the Tri-National Training Program for Psychiatric Genetics (2009–2014) and the Cross-Fertilized Research Training for New Investigators in Egypt and India (2014–2019). A total of 66 trainees, including psychiatrists, psychiatric social workers, clinical psychologists and research psychologists, were supported in research development, which included didactic training, proposal development, hands-on research and manuscript preparation. Methods The aim of this study is to evaluate these three training programmes using the four-level Kirkpatrick Model of Training Evaluation that assesses reaction, learning, behaviour and outcomes. A descriptive analysis was used to explore the data collected throughout the duration of the three training programmes. Online surveys were crafted and sent to the mentors and trainees of the three programmes to supplement objective training data. Results In addition to positive changes in the areas of reaction, learning and behaviour, significant outcomes were demonstrated. As of the writing of this manuscript, the trainees published a total of 130 papers, 59 as first author. In addition, 26 trainees have co-authored papers with one or more trainees or mentors, which demonstrates successful research networking and collaboration. Conclusion Our findings suggest that our training approach is a successful model for building independent mental health researchers. This is a critical step in the development of effective mental health interventions in low- and middle-income countries.

Abstract The persistence of schizophrenia in human populations at a high prevalence and with a large heritability estimate despite reduced fertility and increased mortality rate is a Darwinian paradox. This may be likely if the genomic components that predispose to schizophrenia are also advantageous for the acquisition of important human traits, such as language and cognition. Accordingly, an emerging group of genomic markers of recent evolution in humans, namely human accelerated regions (HARs), since our divergence from chimpanzees, are gaining importance for neurodevelopmental disorders, such as schizophrenia. We hypothesize that variants within HARs may affect the expression of genes under their control, thus contributing to disease etiology. A total of 49 HAR single nucleotide polymorphisms (SNPs) were prioritized from the complete repertoire of HARs (n = 2737) based on their functional relevance and prevalence in the South Asian population. Test of association using 2 independent schizophrenia case-control cohorts of north Indian ethnicity (discovery: n = 930; replication: n = 1104) revealed 3 SNPs (rs3800926, rs3801844, and rs764453) from chromosome 7 and rs77047799 from chromosome 3 to be significantly associated (combined analysis: Bonferroni corrected P < .002–.000004). Of note, these SNPs were found to alter the expression of neurodevelopmental genes such as SLC25A13, MAD1L1, and ULK4; a few from the HOX gene family; and a few genes that are implicated in mitochondrial function. These SNPs may most likely alter binding sites of transcription factors, including TFCP2, MAFK, SREBF2, E2F1, and/or methylation signatures around these genes. These findings reiterate a neurodevelopmental basis of schizophrenia and also open up a promising avenue to investigate HAR-mediated mitochondrial dysfunction in schizophrenia etiology.

Background: Depression is a highly prevalent condition and includes clusters of symptoms, namely, depressive cognition, anxiety, and visceral symptoms. Depressive symptoms often respond sub-optimally to pharmacotherapy. Adjunctive transcranial direct current stimulation (tDCS), a noninvasive brain stimulation modality, may improve depressive symptomatology. Aim: The aim of this study was to study the effect of tDCS as an augmentation strategy in depression and its various symptom domains. Materials and Methods: It is a prospective interventional study. Patients diagnosed with depressive disorder (based on International Classification of Disease- 10 criteria, diagnosed by treating psychiatrist), aged 18-70 years, who showed inadequate improvement on antidepressant selective serotonin reuptake inhibitors, were recruited after informed consent. Each participant was administered 20 sessions of tDCS over 2 weeks, each session of 20 min, with anode placement at left dorsolateral prefrontal cortex and cathode at right supraorbital region. Hamilton Rating Scale for Depression (HAM-D) was administered pre- and post-intervention to assess the change in symptoms. Results: Of a total of 35 participants, the mean score on HAM-D prior to and postintervention was 19.97 (standard deviation [SD] = 3.519) and 13.17 (SD = 3.365), respectively. The difference was statistically highly significant (P = 0.000) on paired t-test. All symptom domains of HAM-D, identified using the Cole and Motivala model (Cole et al., 2004), also showed significant reduction from pre-tDCS to post-tDCS scores (P = 0.000). Conclusion: Positive effect of tDCS on depressive symptoms, its tolerability and safety profile, and affordability makes it an effective therapeutic strategy in augmenting antidepressants in patients with depression. However, longer period studies with larger sample size may yield more generalizable results.

Genetic etiology of schizophrenia is poorly understood despite large genome-wide association data. Long non-coding RNAs (lncRNAs) with a probable regulatory role are emerging as important players in neuro-psychiatric disorders including schizophrenia. Prioritising important lncRNAs and analyses of their holistic interaction with their target genes may provide insights into disease biology/etiology. Of the 3843 lncRNA SNPs reported in schizophrenia GWASs extracted using lincSNP 2.0, we prioritised n = 247 based on association strength, minor allele frequency and regulatory potential and mapped them to lncRNAs. lncRNAs were then prioritised based on their expression in brain using lncRBase, epigenetic role using 3D SNP and functional relevance to schizophrenia etiology. 18 SNPs were finally tested for association with schizophrenia (n = 930) and its endophenotypes—tardive dyskinesia (n = 176) and cognition (n = 565) using a case–control approach. Associated SNPs were characterised by ChIP seq, eQTL, and transcription factor binding site (TFBS) data using FeatSNP. Of the eight SNPs significantly associated, rs2072806 in lncRNA hsaLB_IO39983 with regulatory effect on BTN3A2 was associated with schizophrenia (p = 0.006); rs2710323 in hsaLB_IO_2331 with role in dysregulation of ITIH1 with tardive dyskinesia (p < 0.05); and four SNPs with significant cognition score reduction (p < 0.05) in cases. Two of these with two additional variants in eQTL were observed among controls (p < 0.05), acting likely as enhancer SNPs and/or altering TFBS of eQTL mapped downstream genes. This study highlights important lncRNAs in schizophrenia and provides a proof of concept of novel interactions of lncRNAs with protein-coding genes to elicit alterations in immune/inflammatory pathways of schizophrenia.

Background There is a critical gap between needs and available resources for mental health treatment across the world, particularly in low- and middle-income countries (LMICs). In countries committed to increasing resources to address these needs it is important to conduct research, not only to assess the depth of mental health needs and the current provision of public and private mental health services, but also to examine implementation methods and evaluate mental health approaches to determine which methods are most effective in local contexts. However, research resources in many LMICs are inadequate, largely because conventional research training is time-consuming and expensive. Adapting a hackathon model may be a feasible method of increasing capacity for mental health services research in resource-poor countries. Methods To explore the feasibility of this approach, we developed a ‘grantathon’, i.e. a research training workshop, to build capacity among new investigators on implementation research of Indian government-funded mental health programmes, which was based on a need expressed by government agencies. The workshop was conducted in Delhi, India, and brought together junior faculty members working in mental health services settings throughout the country, experienced international behavioural health researchers and representatives of the Indian Council for Medical Research (ICMR), the prime Indian medical research funding agency. Pre- and post-assessments were used to capture changes in participants’ perceived abilities to develop proposals, design research studies, evaluate outcomes and develop collaborations with ICMR and other researchers. Process measures were used to track the number of single-or multi-site proposals that were generated and funded. Results Participants (n = 24) generated 12 single- or multi-site research grant applications that will be funded by ICMR. Conclusion The grantathon model described herein can be modified to build mental health services research capacity in other contexts. Given that this workshop not only was conceptualised and delivered but also returned results in less than 1 year, this model has the potential to quickly build research capacity and ultimately reduce the mental health treatment gap in resource-limited settings.

Purpose Schizophrenia patients show cognitive and mood impairments, including memory loss and depression, suggesting damage in the brain regions. The hippocampus is a brain structure that is significantly involved in memory and mood function and shows impairment in schizophrenia. In the present study, we examined the regional hippocampal changes in schizophrenia patients using voxel-based morphometry (VBM), Freesurfer, and proton magnetic resonance spectroscopy ( 1 H MRS) procedures. Methods 1 H MRS and high-resolution T1-weighted magnetic resonance imaging were collected in both healthy control subjects ( N  = 28) and schizophrenia patients ( N  = 28) using 3-Tesla whole body MRI system. Regional hippocampal volume was analyzed using VBM and Freesufer procedures. The relative ratios of the neurometabolites were calculated using linear combination model (LCModel). Results Compared to controls, schizophrenia patients showed significantly decreased gray matter volume in the hippocampus. Schizophrenia patients also showed significantly reduced glutamate (Glu) and myo -inositol (mI) ratios in the hippocampus. Additionally, significant positive correlation between gray matter volume and Glu/tCr was also observed in the hippocampus in schizophrenia. Conclusion Our findings provide an evidence for a possible association between structural deficits and metabolic alterations in schizophrenia patients.