Abstract
It has recently been suggested that mood disorders can be characterized by glial pathology as indicated by histopathological postmortem findings. Here, we review studies investigating the glial marker S100B in serum of patients with mood disorders. This protein might act as a growth and differentiation factor. It is located in, and may actively be released by, astro- and oligodendrocytes. Studies consistently show that S100B is elevated in mood disorders; more strongly in major depressive than bipolar disorder. Successful antidepressive treatment reduces S100B in major depression whereas there is no evidence of treatment effects in mania. In contrast to the glial marker S100B, the neuronal marker protein neuron-specific enolase is unaltered. By indicating glial alterations without neuronal changes, serum S100B studies confirm specific glial pathology in mood disorders in vivo. S100B can be regarded as a potential diagnostic biomarker for mood disorders and as a biomarker for successful antidepressive treatment.
Highlights
It has recently been suggested that mood disorders can be characterized by glial pathology as indicated by histopathological postmortem findings
Specific reductions in oligodendrocytes have been reported for the amygdala in major depressive disorder (MDD) [14], and microglial alterations in bipolar disorder (BD), including manic episodes [1]
Previous studies have shown that S100B, which is found in astro- and oligodendroglia, but not in microglia in the human brain [19], is altered in both serum [20, 21] and cerebrospinal fluid in mood disorders
Summary
Mood disorders—once considered “good prognosis diseases” —have, a less favorable outcome than previously thought [1, 2]. Rajkowska’s hypothesis [3] of glial pathology in mood disorders has been supported by a recent study that ablated astroglial cells in the prefrontal cortex of adult rats pharmacologically with L-alpha-aminoadipic acid (L-AAA) [17]. Antidepressive treatment has been shown to successfully reverse reduction in astroglial density in animal models of depression [18]. Density and size of cortical neurons are reduced in the orbitofrontal and dorsolateral prefrontal cortices in mood disorders, these neuronal reductions seem less pronounced than glial alterations and are detected only when specific morphological size-types of neurons are analyzed in individual cortical layers [1, 6]
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