Translational developmental psychiatry最新文献

{"title":"FCAP 2015","authors":"","doi":"10.3402/tdp.v3.29697","DOIUrl":"https://doi.org/10.3402/tdp.v3.29697","url":null,"abstract":"","PeriodicalId":90753,"journal":{"name":"Translational developmental psychiatry","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3402/tdp.v3.29697","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69950933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Manualized social skills group training for children and adolescents with higher functioning autism spectrum disorder: protocol of a naturalistic multicenter, randomized controlled trial","authors":"Nora Choque Olsson, K. Tammimies, S. Bölte","doi":"10.3402/tdp.v3.29825","DOIUrl":"https://doi.org/10.3402/tdp.v3.29825","url":null,"abstract":"Autism spectrum disorder (ASD) is a lifelong neurodevelopmental disorder characterized by impairments in social communication and interaction, and the presence of stereotyped, repetitive and restricted behavior, interests, and activities. Despite prior studies showing moderate efficacy of social skills group training (SSGT) for children and adolescents with ASD, its effectiveness remains unclear. To investigate the efficacy and effectiveness of SSGT, we have initiated a large randomized controlled multicenter trial of the manualized SSGT program ‘KONTAKT’ in N=288 children and adolescents with high functioning ASD and psychiatric comorbidities (attention deficit hyperactivity disorder, anxiety, and depression) recruited from 14 clinical units. Based on stratification for age group (children vs. adolescents) and lengths of intervention (short vs. long), the participants are randomly assigned to SSGT KONTAKT training (n=144) or to treatment as usual (n=144). Outcomes are assessed by blinded teachers and unblinded parents on the Social Responsiveness Scale (primary outcomes), participant's self-reports, and clinician ratings using well-established instruments for adaptive skills, general psychopathology, and experienced stress (secondary outcomes). We expect that participants receiving SSGT KONTAKT will show improved social responsiveness and everyday functioning, decreased general symptom severity, and perceived stress compared to standard care. Moreover, we predict that participant characteristics such as genetic predisposition, age, IQ, sex, verbal skills, and comorbidity moderate treatment effects.","PeriodicalId":90753,"journal":{"name":"Translational developmental psychiatry","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3402/tdp.v3.29825","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69950978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A neuroconstructivistic research strategy to study the underlying causes of dyslexia","authors":"M. Trautmann","doi":"10.3402/tdp.v2.21684","DOIUrl":"https://doi.org/10.3402/tdp.v2.21684","url":null,"abstract":"The present article suggests an extended neuroconstructivistic research strategy for assessing the causes of dyslexia. Instead of following one line of argumentation, such as the influence of auditory perception on the development of phonological awareness, a systematic facet model is suggested to identify the development of singular, bi-, and cross-modal perception, attention, and higher cognition in dyslexia over time. In addition, such a study should also include etiological measures such as genetic and family risk factors. This developmental approach is necessary to suggest a pragmatic concept for investigating all processing types of dyslexia under several methodological aspects.","PeriodicalId":90753,"journal":{"name":"Translational developmental psychiatry","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3402/tdp.v2.21684","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69950162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetics of antipsychotic drug outcome and implications for the clinician: into the limelight","authors":"Amtul H. Changasi, T. Shams, Jennie G Pouget, D. Müller","doi":"10.3402/tdp.v2.24663","DOIUrl":"https://doi.org/10.3402/tdp.v2.24663","url":null,"abstract":"Background and purpose Antipsychotics (APs) are the primary method of treatment for schizophrenia and other psychotic disorders. Unfortunately, lengthy trial-and-error approaches are typically required to find the optimal medication and dosage due to a large interindividual variability with outcome to AP treatment. The literature has shown abundant evidence for a genetic component in individuals’ responses to APs. Pharmacogenetic studies analyze specific genetic markers and their association with symptom improvement and occurrence of side effects with APs. This research aims to optimize AP drug treatment by usage of predictive testing and to personalize medicine. Recent findings This review will highlight the most consistent findings in pharmacogenetics of APs and will update the reader on the clinical implications. This will include how genetic variants modulate AP drug levels, side effects, and therapeutic symptom improvement (i.e. response) to AP treatment. Summary Several promising findings were obtained implicating gene variants of the dopamine receptor genes in addition to gene variants of serotonin receptors for response and common side effects. Notably, effect sizes appear to be particularly high in the genetics of side effects compared to response. One example is antipsychotic-induced weight gain where the leptin, HTR2C and in particular the melanocortin-4-receptor (MC4R) genes have been implicated in weight gain in children and adolescents. Consistent findings were also obtained for genes implicated in tardive dyskinesia and agranulocytosis. However, the most clinically relevant findings pertain to genes involved in drug metabolism such as the CYP2D6 and CYP2C19 genes which have been included in the first genetic test kits such as the Amplichip® CYP450 Test and more recently the DMET™ Plus Panel, the Genecept™ Assay, the Genomas HILOmet PhyzioType™ System, and the GeneSight® Test.","PeriodicalId":90753,"journal":{"name":"Translational developmental psychiatry","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3402/tdp.v2.24663","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69950762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum: Genetics of antipsychotic drug outcome and implications for the clinician: into the limelight","authors":"","doi":"10.3402/tdp.v2.25715","DOIUrl":"https://doi.org/10.3402/tdp.v2.25715","url":null,"abstract":"","PeriodicalId":90753,"journal":{"name":"Translational developmental psychiatry","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3402/tdp.v2.25715","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69950677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Treatment experiences of males with an eating disorder: a systematic review of qualitative studies","authors":"Priyanka Thapliyal, P. Hay","doi":"10.3402/tdp.v2.25552","DOIUrl":"https://doi.org/10.3402/tdp.v2.25552","url":null,"abstract":"Research has commonly examined eating disorders (EDs) predominantly in female groups. However, males are a large minority of people with EDs. In view of this, the present paper aimed to investigate and review the experience of treatment and recovery for males with an ED. We carried out a systematic search for qualitative articles focusing on the experiences of treatment and found only four papers which met inclusion criteria. Key themes identified across studies were 1) delays in seeking treatment, 2) clinical features distinctive to males such as drive for muscularity, 3) feminine and other aspects of treatment services, and 4) lack of consensus in views about relevance of sex in treatment. More studies are needed to explore male pathways through treatment and both impediments, but also facilitators, of successful engagement in and response to treatment.","PeriodicalId":90753,"journal":{"name":"Translational developmental psychiatry","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3402/tdp.v2.25552","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69950626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serotonin transporter genotype modulates HPA axis output during stress: effect of stress, dexamethasone test and ACTH challenge.","authors":"Andrea N Sorenson, Erin C Sullivan, Sally P Mendoza, John P Capitanio, J Dee Higley","doi":"10.3402/tdp.v1i0.21130","DOIUrl":"10.3402/tdp.v1i0.21130","url":null,"abstract":"<p><strong>Background: </strong>Studies show that the hypothalamic-pituitary-adrenal (HPA) axis is dysregulated in depression. Some studies suggest that variation in the serotonin transporter genotype (hereafter <i>5HTT</i>) modulates both risk for depression and psychopathological HPA axis responsiveness. Rhesus monkeys are well suited to model such relationships. Rhesus macaque models of human psychopathology have assessed the effect of the serotonin transporter (<i>rh5HTT</i>) on levels of cortisol in stressed subjects. These studies show that that under conditions of stress, heterozygous females (Ls) reared under adversity exhibit high levels of cortisol. Studies have not to our knowledge, however, assessed the potential additive effect on the cortisol response in a number of macaque subjects homozygous for the serotonin transporter short allele (ss). Moreover, little is known about the level of the central or peripheral nervous system at which the <i>5HTT</i> genotype acts to modulate the cortisol response.</p><p><strong>Methods: </strong>This study assesses a relatively large number of subjects homozygous and heterozygous for the <i>rh5HTT</i> short and long alleles (a) during stress; (b) following a dexamethasone suppression test; and (c) following an adrenocorticotropic hormone (ACTH) challenge. Subjects included 190 infant rhesus macaques (<i>Macaca mulatta</i> - 84 males and 106 females; 118 LL, 60 Ls, and 12 ss subjects), obtaining two blood plasma samples during the stress of separation from their mothers. Then on the following day, we obtained a blood sample following a dexamethasone test, and later that day we obtained a blood sample after an ACTH challenge test. Subjects ranged in age between 90 and 128 days, with a mean age of 107 days.</p><p><strong>Results: </strong>Subjects homozygous for the short allele had significantly higher levels of cortisol across all test conditions, when compared to those homozygous for the long allele, or those heterozygous with Ls alleles. Subsequent analyses showed a high correlation between individual cortisol levels across the three different tests.</p><p><strong>Conclusions: </strong>These data suggest that subjects homozygous for the short allele are more likely to show dysregulated cortisol levels in response to stress. Given the correlation in individual responses of the HPA axis across the different tests, our data suggest that the effect of the <i>5HTT</i> genotype shows some commonality in its regulation of stress, feedback, and ACTH-stimulated cortisol output. Our data suggest that under conditions of stress, the serotonin transporter may modulate HPA axis psychopathology.</p>","PeriodicalId":90753,"journal":{"name":"Translational developmental psychiatry","volume":"1 ","pages":"21130"},"PeriodicalIF":0.0,"publicationDate":"2013-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/33/1d/nihms558321.PMC4109987.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32539945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential Effects of Tryptophan Challenge on Mood and Coping with Stress in Subjects with Genetic (5-HTTLPR) or Chronic Stress-Induced Brain 5-HT Vulnerabilities","authors":"R. Markus","doi":"10.3402/TDP.V1I0.19055","DOIUrl":"https://doi.org/10.3402/TDP.V1I0.19055","url":null,"abstract":"Background Brain serotonin (5-HT) dysfunction is a relevant pathophysiological factor contributing to stress proneness and hence to stress-related affective disturbances. Susceptibility to 5-HT dyfunction, 5-HT vulnerability, is not only promoted by cognitive proneness (frequent stress perceptions and experiences) but also by genetic vulnerabilities. A commonly recognized 5-HT vulnerable genotype involves a polymorphism in the 5-HT transporter-linked promoter region (5-HTTLPR). This region encodes the 5-HT transporter protein (5-HTT), controls 5-HT reuptake and function, and is the target mechanism for antidepressant drugs. The short-allele (S) variant 5-HTTLPR is associated with lower 5-HTT mRNA concentrations than the long-allele (L) variant and is thought to promote 5-HT vulnerability for the negative affective effects of stress. Brain 5-HT vulnerabilities are often explored by tryptophan depletion (ATD). This intervention reduces brain 5-HT by lowering the plasma dietary amino acid tryptophan, the precursor of 5-HT, which competes with other large neutral amino acids (TRP/LNAA ratio) for uptake into the brain. Yet, because 5-HT vulnerable subjects may exhibit enhanced post-synaptic sensitization, as a compensatory response to reduced 5-HT availability and/or lower pre-synaptic 5HTT expression, they may be particularly susceptible for the beneficial effects of tryptophan challenge. Data showing that cognitive and/or genetically 5-HT vulnerable subjects are indeed less affected by the negative effects of acute stress exposure following dietary tryptophan augmentation will be presented.","PeriodicalId":90753,"journal":{"name":"Translational developmental psychiatry","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3402/TDP.V1I0.19055","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69949908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Use of Acute Tryptophan Depletion in Children and Adolescents","authors":"F. Zepf","doi":"10.3402/TDP.V1I0.18393","DOIUrl":"https://doi.org/10.3402/TDP.V1I0.18393","url":null,"abstract":"The neurotransmitter serotonin (5-HT) plays an important role in many neuropsychiatric disorders, in particular affective disorders, eating disorders and disorders related to problems in processing emotions. Different methods have been applied in previous studies on adults to investigate central nervous serotonergic neurotransmission. Acute tryptophan depletion (ATD) is a neurodietary method to reduce central nervous serotonin synthesis in humans for a short period by decreasing the availability of the amino acid tryptophan, TRP, the physiological precursor to 5-HT. Uptake of endogenous TRP into the central nervous system is decreased by a reduced transport of TRP over the blood–brain barrier as TRP competes with other amino acids administered to the subjects within an amino acid beverage lacking TRP after an overnight fast. According to previous studies, frequent side effects of using ATD in adults are vomiting and nausea, thus limiting its use. Here, we present a modified ATD protocol that was adapted for use in children and adolescents, with the administration of an amino acid beverage adapted to the body weight of the subjects. Underlying principles of this ATD modification termed Moja-De and first research findings based on this ATD formulation will be presented and discussed.","PeriodicalId":90753,"journal":{"name":"Translational developmental psychiatry","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69949810","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Placental tryptophan metabolism as a potential novel pathway for the developmental origins of mental diseases","authors":"N. Goeden, J. Velásquez, A. Bonnin","doi":"10.3402/tdp.v1i0.20593","DOIUrl":"https://doi.org/10.3402/tdp.v1i0.20593","url":null,"abstract":"Dysfunction of brain serotonin (5-HT) signaling contributes to the pathophysiology of several psychiatric disorders. However, before 5-HT acts as a neurotransmitter/neuromodulator in the adult brain, increasing evidence suggests that it plays crucial roles in the modulation of essential neurodevelopmental processes. It was recently demonstrated that the placenta synthesizes 5-HT from maternally derived tryptophan during pregnancy. Therefore, genetic and environmental perturbations that affect placental tryptophan metabolism could alter neurodevelopmental processes in the developing embryo, and contribute to the developmental origin of psychiatric disorders. Here we discuss how disruptions of the placental tryptophan metabolic pathway may lead to abnormal brain development and function in adult life.","PeriodicalId":90753,"journal":{"name":"Translational developmental psychiatry","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3402/tdp.v1i0.20593","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69950030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}