The role of damage associated molecular pattern molecules (DAMPs) and permeability of the blood-brain barrier in depression and neuroinflammation.

Depression is a heterogeneous mental disorder characterized by feelings of sadness and loss of interest that render the subject unable to handle basic daily activities such as sleeping, eating, or working. Neurobiological traits leading to depression include genetic background, early life abuse, life stressors, and systemic and central inflammatory profiles. Several clinical and preclinical reports documented that depression shows an increase in pro-inflammatory markers such as interleukin (IL-)1β, IL-6, IL-12, tumor necrosis factor (TNF), and interferon (IFN)-γ; and a decrease in anti-inflammatory IL-4, IL-10, and transforming growth factor (TGF)-β species.

Hippocampal volume as treatment predictor in antidepressant naïve patients with major depressive disorder.

Major depression disorder (MDD) limits psychosocial functioning and quality of life. One of the biological alterations is a hippocampal volume (HV) reduction. Previous prospective neuroimaging studies present inconsistencies regarding HV reductions and clinical features and response of antidepressant treatment of the participants.

[Response to serotonergic and noradrenergic antidepressants: a crossover study of fluoxetine and desipramine in patients with first major depression episode].

Background: Response rate data from studies with different kinds of antidepressant drugs help in the development of guidelines for the rational prescription of pharmacotherapy. However, there are still few comparative studies with selective reuptake inhibition on serotonin or norepinephrine in the same sample of major depression patients.

Methods: First episode major depression (DSM-III-R) outpatients who completed 6 weeks in two double-blind randomized trials with fluoxetine and desipramine were crossed over to treatment with the other drug under open conditions for 6 weeks.