Exploring glia in schizophrenia and depression
In recent years, researchers in the neurosciences have changed their focus of attention from neurons to glia. This “glial turn” has revealed new approaches and hypotheses for the healthy brain and its disorders. Recently, mood disorders, namely major depression, have been described as diseases mainly affecting glia and particularly astrocytes. We have validated the glial hypothesis of mood disorders in humans by measuring serum markers with meta-analyses, and cell culture models. We were able to show that the glial marker protein S100B is elevated in major depression. These elevations seem to be related to the severity of depression and might be used as treatment markers. In contrast, the neuronal marker protein neuron-specific enolase (NSE) is unchanged. However, increases of S100B are not specific for mood disorders. We and others detected the same alterations in schizophrenia that were particularly related to the “deficit syndrome” characterized by “negative symptoms”. Now, cell culture models of astrocytes, which we have also previously used to investigate the blood-brain barrier, are underway exploring drug effects specifically.
Elevated serum levels of the glial marker protein S100B are not specific for schizophrenia or mood disorders. Molecular Psychiatry 14(2009): 235-237. IF 12.5
NSE is unaltered whereas S100B is elevated in serum of patients with schizophrenia – Original research and meta-analysis.Psychiatry Research 167(2009): 66-72. IF 2.3
Serum markers support disease-specific glial pathology in major depression. Journal of Affective Disorders 111(2008): 271-280. IF 3.1
Das antioxidative System der Blut-Hirn-Schranke - Einfluß von Astrozyten sowie Hypoxie/Reoxygenierung.(The antioxidative system of the blood-brain barrier – influences of astrocytes and hypoxia/reoxygenation) Shaker-Verlag, Aachen, Germany, 2005. ISBN 978-3-8322-4626-6.
Serum S100B is increased during early treatment with antipsychotics and in deficit schizophrenia. Schizophrenia Research 62(2003): 231-236. IF 3.9