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Background: Numerous studies have reported associations between the brain-derived neurotrophic factor (BDNF) gene and psychiatric disorders, including suicidal behavior, although with conflicting results. Methods: A total of 250 major depressive disorder patients were collected in the context of a European multicenter resistant depression study and treated with antidepressants at adequate doses for at least 4 weeks. Suicidality was assessed using the Mini International Neuropsychiatric Interview and Hamilton Rating Scale for Depression, and treatment response using the HAM-D. Genotyping was performed for the functional Val66Met polymorphism (rs6265) and 7 additional tagging single nucleotide polymorphisms within the BDNF gene. Results: Neither BDNF single markers nor haplotypes were found to be associated with suicide risk and lifetime history of suicide attempts. Gender-specific analyses revealed nonsignificant single marker (rs908867) and haplotypic association with suicide risk in males after multiple testing correction. Analyzing treatment response phenotypes, the functional Val66Met polymorphism as well as rs10501087 showed significant genotypic and haplotypic association with suicide risk in remitters (n = 34, 13.6%). Conclusions: Considering the sample size, the present findings need to be replicated in larger samples to confirm or refute a role of BDNF in the investigated suicidal behavior phenotypes., SCOPUS: ar.j, info:eu-repo/semantics/published

Co-morbid physical illness has been suggested to play an important role among the factors contributing to treatment resistance in patients with major depressive disorder. In the current study we compared the rate of physical co-morbidity, defined by ICD-10, among a large multicenter sample of 702 patients with major depressive disorder. A total of 356 of the participants were defined as treatment resistant depression (TRD) patients-having failed two or more adequate antidepressant trials. No significant difference was found between TRD and non-TRD participants in the prevalence of any ICD-10 category. This finding suggests that although physical conditions such as diabetes, thyroid dysfunction, hypertension, ischemic heart disease, and peptic diseases are often accompanied by co-morbid MOD, they do not necessarily have an impact on the course of MOD or the likelihood to respond to treatment. Marginally higher rates of co-morbid breast cancer, migraine and glaucoma were found among TRD participants. Possible explanations for these findings and their possible relation to TRD are discussed. (C) 2012 Elsevier B.V. and ECNP. All rights reserved.

Social anxiety disorder (SAD) is considered to be one of the most common anxiety disorders. Despite its high prevalence, the disorder is still considerably underdiagnosed and undertreated. SAD shows a typically early onset in childhood or early adolescence and generally becomes chronic. The disease places a massive burden on patients lives, affecting not only their social interactions but also their educational and professional activities, thereby constituting a severe disability. Although substantial progress in the study of the etiology of SAD has been made, no commonly accepted model has emerged yet. Data from genetic and neuroimaging studies point towards a contribution of several neurotransmitter systems (i.e. norepinephrine, dopamine and serotonin) to the pathophysiology of this disorder. Functional magnetic resonance imaging studies have repeatedly emphasized the central role of the amygdalae and insula in the neural circuitry of the disorder. Selective serotonin reuptake inhibitors (SSRI) are commonly accepted as first line therapy, however other substance classes like serotonin norepineprine reuptake inhibitors (SNRI), monoamine oxidase inhibitors (MAOI), benzodiazepines and several other agents have also proved effective. There is still a substantial lack of data on therapeutic options in cases of non-responsive SAD as well as on add-on therapy. A combined treatment-approach including psychotherapy (e.g. cognitive behavioural therapy) may prove useful., Sozialphobien gehören zu den häufigsten psychiatrischen Erkrankungen. Ungeachtet der hohen Prävalenz wird diese Erkrankung noch immer zu selten erkannt, diagnostiziert und und ausreichend behandelt. Das Krankheitsbild entwickelt sich typischerweise in der Kindheit oder im frühen Adoleszenzalter und zeigt häufig einen chronischen Verlauf. Die Erkrankung stellt eine massive Belastung für die Patienten dar und wirkt nicht nur in sozialen Aspekten, sondern auch im Beruf und der Ausbildung der Betroffenen behindernd. Obwohl in der Erforschung der Ätiologie der Erkrankung bereits große Fortschritte gemacht wurden, hat sich noch kein allgemein akzeptiertes Modell entwickelt. Die Daten aus genetischen Studien und Studien mit bildgebenden Verfahren deuten auf ein Mitwirken des noradrenergen, des dopaminergen und des serotonergen Systems in der Pathophysiologie hin. In funktionellen Magnetresonanztomographiestudien wurde wiederholt die zentrale Rolle von Strukturen wie den Amydalae und der Insula in der neuronalen Grundlage der Sozialphobien gezeigt. In der Therapie der Sozialphobien werden allgemein selekive Serotonin- Wiederaufnahmehemmer als Mittel der ersten Wahl betrachtet. Andere Substanzklassen wie Serotonin-Noradrenalin-Wiederaufnahmehemmer, Monoaminoxidasehemmer, Benzodiazepine und einzelne andere Psychopharmaka haben ebenfalls Therapieeffizienz bewiesen. Zum gegenwärtigen Zeitpunkt gibt es noch immer kaum Daten über Therapieoptionen bei Therapieresistenz oder über add-on Strategien. Eine weitere Möglichkeit stellen kombinierte Therapiestrategien mit psychotherapeutischen Ansätzen (z.B. kognitive Verhaltenstherapie) dar.

Materials and methods Eighteen healthy female subjects participated in this PET study. The selective 5-HT1A receptor antagonist [carbonyl-11C]WAY-100635 was used as radioligand. The hypothalamus as an essential part of the HPA axis and eight control regions of interest and the cerebellum as reference region were defined a priori and delineated on coregistered MR images. DHEAS and cortisol plasma levels were ascertained by morning blood collections on the PET day. The 5-HT1A receptor binding potentials of the target brain regions were correlated with DHEAS, cortisol plasma levels and the ratio of DHEAS / cortisol.