Are Transcriptional Responses to Inbreeding a Functional Response to Alleviate Inbreeding Depression?

Are transcriptional responses to inbreeding a functional response to alleviate inbreeding depression?

Fly (Austin). 2013 Jan 1; 7(1): 8-12
García C, Avila V, Quesada H, Caballero A

Previous studies addressing the relationship between gene regulation and inbreeding depression did not allow for discerning the changes that alleviate the depression from those that generate it. We directly addressed this question by analyzing changes in gene expression, using Affymetrix 2.0 arrays in Drosophila melanogaster inbred sublines differing in their magnitudes of inbreeding depression relative to the expression in an outbred control. The total number of arrays analyzed was 27, with 9,133 probe sets showing a significant signal of expression. We found that for those genes differentially expressed between inbred and outbred sublines, most of them showed a pattern of expression consistent with a protective role against inbreeding effects. The observed increase in depression was presumably related to an inability of the genome to do the appropriate expression adjustments. Expression changes detected in our study showed a clear specificity of RNA-splicing and energy derivation functions. Thus, it appears that most of the observed changes in gene expression associated with inbreeding may occur predominantly to alleviate inbreeding depression, i.e., as a protection against the effects of inbreeding. HubMed – depression

Clinical and neurohormonal correlates and prognostic value of serum prolactin levels in patients with chronic heart failure.

Eur J Heart Fail. 2013 May 2;
Parissis JT, Farmakis D, Fountoulaki K, Rigas A, Nikolaou M, Paraskevaidis IA, Bistola V, Venetsanou K, Ikonomidis I, Anastasiou-Nana M, Kremastinos DT, Filippatos G

AIMS: Hypothalamic axis deregulation is associated with clinical severity and depression in chronic heart failure (CHF). We investigated the relationship of serum prolactin, an indicator of hypothalamic axis function, to neurohomonal/immune activation and depressive symptoms in CHF as well as its prognostic value. METHODS AND RESULTS: Serum prolactin was determined in 180 patients with advanced CHF (aged 65 ± 12 years, mean LVEF 27 ± 7%) along with natriuretic peptides (BNP), inflammatory cytokines, endothelial adhesion molecules, 6 min walk test (6MWT), and the Zung self-rating depression scale (SDS). Patients were followed for all-cause death or hospitalization for cardiovascular reasons for up to 8 months. Prolactin levels were significantly correlated with NYHA class (r = 0.394, P < 0.001), LVEF (r = -0.314, P < 0.001), 6MWT (r = -0.353, P < 0.001), BNP (r = 0.374, P < 0.001), Zung SDS (r = 0.544, P < 0.001), interleukin-6 (IL-6) (r = 0.451, P < 0.001), IL-10 (r = -0.426, P < 0.001), tumour necrosis factor (TNF)-? (r = 0.310, P = 0.001), soluble Fas (r = 0.333, P < 0.001), soluble Fas-ligand (r = 0.517, P < 0.001), soluble intercellular adhesion molecule-1 (ICAM-1) (r = 0.409, P < 0.001), and soluble vascular cell adhesion molecule-1 (VCAM-1) (r = 0.480, P < 0.001). During follow-up, 119 patients (66%) died or were hospitalized for cardiovascular events after a median time of 72 days (range 5-220 days); these patients had higher baseline prolactin levels (10.2 ± 5.7 vs. 6.7 ± 4.3 ng/mL, P < 0.001), and a prolactin value ?4.5 ng/mL was associated with a higher rate of death or hospitalization (116 ± 7 vs. 181 ± 11 days, P = 0.0001). In multivariate analysis, prolactin levels remained an independent predictor of death or hospitalization (<4.5 vs. ?4.5 ng/mL; odds ratio, 0.368; 95% confidence interval 0.148-0.913; P = 0.031), along with BNP (P < 0.001) and 6MWT (P = 0.020). CONCLUSIONS: Serum prolactin is associated with neurohormonal/immune activation and depressive symptoms and is an independent predictor of prognosis in advanced CHF. HubMed – depression

Oligodendrocyte density is changed in the basolateral amygdala in schizophrenia but not depression.

Schizophr Res. 2013 Apr 29;
Williams MR, Harb H, Pearce RK, Hirsch SR, Maier M

HubMed – depression

Malaise, Melancholia and Madness: The Evolutionary Legacy of an Inflammatory Bias.

Brain Behav Immun. 2013 Apr 29;
Raison CL, Miller AH

Evolutionary imperatives bred a vigorous and highly orchestrated behavioral and immune response to the microbial world that served to promote species survival and propagation. The resultant legacy is an inflammatory bias which goes largely unchecked in the modern world and is provoked not only by pathogens but also now by people. In this commentary, the authors’ contributions to the Special Issue on Inflammation and Mental Health are described, beginning with the origins of the inflammatory bias, its roots in genetic predispositions to behavioral adaptations and ultimately maladaptations, and its consequences on the developing brain. In addition, the mechanisms by which the immune system engages behavior are described including a central role for the inflammasome which may serve to link psychological stress with inflammatory and behavioral responses. Neurotransmitter systems that mediate effects of the immune system on behavior are also described along with interactions of the inflammatory bias with depression and their convergent impact on the response to stress and medical illness. Finally, translational implications are discussed including data from a clinical trial using a cytokine antagonist in depressed patients, which suggests an interaction of the inflammatory bias with other evolutionary legacies including those related to food consumption and their modern consequences of obesity and the metabolic syndrome. Taken together, the articles offer a sampling of the rich literature that has evolved regarding the role of the immune system in behavioral disorders. The grounding of this relationship in our evolutionary past may serve to inform future research both theoretically and therapeutically. HubMed – depression