Dear colleagues,
It is my great pleasure to welcome you to our last issue of 2013 featuring up-to-date research on biological markers in alcoholism and in mood disorders as well as on cognitive and biological characteristics of eating disorders.
The WFSBP consensus paper by Hashimoto and colleagues presents an overview of current literature on biological markers for alcoholism, including markers associated with the pharmacological effects of alcohol and markers related to the clinical course and treatment of alcohol-related problems. The article emphasizes the role of biomarkers not only in diagnosis, but also in predicting prognosis, disease progression, development of new treatments and monitoring treatment effects.
Sjoerds and colleagues addressed the question whether gray matter abnormalities that are associated with alcohol-use disorders are also found in non-alcoholics with familial alcohol dependence. The authors indeed found abnormalities in the parahippocampal gyrus in these subjects, which may be interpreted as persistent biological susceptibility for alcohol dependence or related psychopathology and not neurotoxity of alcohol or delayed brain maturation.
In their genome-wide association study (GWAS), Galfalvy and colleagues sought for genes related to suicide with and without major depression. Ninety-nine subjects, including 68 who completed suicide, were genotyped post mortem. The analysis revealed 58 SNP’s, 22 of them in or near 19 known genes with the diagnosis of mood disorder not explaining the associations. Moreover, seven genes showed altered expression in suicides as compared with controls, especially in immune system-related genes, which may highlight a role for neuroimmunological effects in suicidal behaviour.
By combining methods of a meta-analysis and a GWAS, Terracciano and colleagues set out to identify genetic variants associated with serum brain-derived neurotrophic factor (BDNF), one of the best known biological markers of depression. Their results revealed that the BDNF Val66Met variant is not associated with serum BDNF, but other variants in the BDNF and NTRK3 genes might regulate the level of serum BDNF.
More recently, greater 5-HT2CR editing was found in suicide victims with prior bipolar disorder or schizophrenia, so Lyddon and colleagues set out to compare suicides and non-suicides with major depressive disorder (MDD) and non-suicide healthy controls. Their findings suggest the presence of two factors associated with 5-HT2CR editing, one of them is linked to MDD and is associated with less editing, the other is linked to suicide alone and is associated with more editing and, therefore, less receptor function.
By applying the place-avoidance task with rats, Perera and colleagues addressed the question whether neurogenesis improves mood by facilitating segregation of novel experiences that conflict with older maladaptive memories. Results revealed that stressed rats treated with placebo were slower in learning and had lower neurogenesis rates than stressed rats given a drug and non-stressed animals. The authors interpret these findings in the light of the theory on increasing neurogenesis enhancing acquisition of novel experiences by suppressing activation of mature hippocampal neurons that mediate established, conflicting memories.
Schosser and colleagues set out to identify genes contributing to co-occurring anxiety in MDD. The authors examined a total of 1522 MDD cases with and without anxiety, and compared them to 1588 healthy controls at a genome-wide level. Although suggestive evidence was found for several SNP's, the authors’ findings suggest that there are no common genetic variants strongly associated with anxious depression.
Introducing our last topic, cognitive and biological characteristics of eating disorders, Paszynska and colleagues investigated whether vomiting bulimic and/or non-bulimic depressive patients treated with fluoxetine have altered proportions of inorganic components in their parotid salivary gland secretions compared to healthy controls. Their results indicated a reduction in flow and sodium and potassium ions in the parotid saliva in bulimic patients and a reduction in flow in non-bulimic patients treated with fluoxetine. Deficits in certain components of saliva were shown to be directly related to salivary flow rate.
Finally, Cardi and colleagues set out to investigate the attentional bias to facial stimuli in patients with a lifetime diagnosis of either anorexia nervosa or bulimia nervosa. In addition to 50 healthy controls, they tested 46 patients with current eating disorders and 22 participants recovered from eating disorders with a social dot-probe task. The authors found that participants with a lifetime diagnosis of an eating disorder show an attentional bias to rejecting faces and a difficulty in disengaging attention from these stimuli, which may contribute to the causation or maintenance of the illness.
Yours sincerely,
Siegfried Kasper, MD
Chief Editor