Dear colleagues,
It is my great pleasure to welcome you to the eighth issue of 2012.
In this year's last issue, we will present current work on the identification of biological alterations in affective disorders. A focus is set on exploring characteristics that are present prior to clinical manifestation of psychiatric symptoms, i.e. neuro psychological, neuroanatomical, metabolic and genomic biomarkers, as they can be seen as the cornerstones of a preventive and personalized psychiatry of the future.
Bosch and colleagues start off with a review on current concepts on neuroendocrine and genetic principles underlying stress-related depression and discuss their interactions with pharmacological treatment. They emphasize the need of further research to minimize heterogeneity in the depression phenotype, to detect biologically characterized subgroups of patients and to identify genetic and functional predictors of antidepressant treatment response.
The interplay of genetic and early environmental factors is considered to play an important role in the aetiology of major depressive disorder (MDD). Carballedo and colleagues broaden existing knowledge with their finding that individuals at high genetic risk of suffering MDD have reduced volumes of brain regions related to emotional processing in particular when they additionally suffered early life adversity.
Kim and colleagues investigated the association between cytokine gene polymorphisms and post-stroke depression and report that susceptibility to developing depression within two weeks after stroke is higher in patients with alleles related to lower anti-inflammatory cytokine production.
In a six-year follow-up study, Milaneschi and colleagues found a relationship between the presence of depressive symptoms and low plasma concentrations of carotenoids indicating fruit and vegetable intake, which was partially mediated by serum inflammatory markers in older people.
The fibroblast growth factor receptor 2 (FGFR2) gene is located on chromosome 10q25-q26, a hot linkage region for both schizophrenia (SCZ) and bipolar disorder (BD). A large scale case-control study by Wang and colleagues now revealed a specific association of FGFR2 with BD, which was not present for patients with SCZ or MDD.
Current models of BD focus on a dysfunction within prefrontal cortical regions involved in cognitive control coupled with overactivity within subcortical structures implicated in emotional processing. Using functional magnetic resonance imaging (fMRI) in euthymic patients with BD, Jogia and colleagues found that this activation pattern is present even in tasks that do not typically engage emotional systems.
Aside from findings on reduced brain activations, little is known about de-activations during performance on cognitive tasks in BD. Pomarol-Clotet and colleagues aimed to bridge this gap and report results on a failed de-activation in the medial frontal cortex during performance of a working memory task in manic patients with BD.
In a brief report, Schwarz and colleagues show their results on the presence of distinct patterns of multiple molecular biomarkers in serum even before the stage in which symptoms are first manifested in SCZ and BD.
Yours sincerely,
Siegfried Kasper, MD
Chief Editor