Serum markers support disease-specific glial pathology in major depression

Background ly, it was shown by histopathological studies that mood disorders are characterized by disease-specific glial pathology. s idate this hypothesis in vivo we measured weekly and simultaneously serum levels of the neuronal marker neuron-specific enolase and S100B, a protein expressed in astro- and oligodendroglia in the human brain, in 10 patients with major depressive disorder and 10 age- and gender-matched control subjects. Furthermore, we conducted a systematic, quantitative meta-analysis of all published studies on S100B involving 193 patients suffering from mood disorders and 132 healthy control subjects by calculating effect sizes. s was elevated at admission and discharge in our patients with major depression compared with control subjects, whereas there were no significant differences for neuron-specific enolase. During treatment S100B decreased slightly, although this effect was not significant. It had no significant impact on neuron-specific enolase. The meta-analysis revealed that serum levels of S100B are consistently elevated in mood disorders during acute major depressive or manic episodes. Additionally, it demonstrated that serum S100B decreases during antidepressive treatment reliably if clinical improvement is sufficient. tions study measured only serum S100B, future (cell culture) studies have to elucidate molecular mechanisms of this protein in mood disorders. Moreover, results have to be replicated in a larger patient group. sions may represent a biomarker for mood disorders, particularly major depression, and their treatment. Together with unaltered levels of neuron-specific enolase, our results support in vivo the histopathologically generated hypothesis of disease-specific glial pathology in mood disorders.