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First evidence for glial pathology in late life minor depression: S100B is increased in males with minor depression.

Polyakova M, Sander C, Arelin K, Lampe L, Luck T, Luppa M, Kratzsch J, Hoffmann KT, Riedel-Heller S, Villringer A, Schoenknecht P, Schroeter ML - Front Cell Neurosci (2015)

Bottom Line: S100B was significantly increased in males with minor depression in comparison to healthy males, whereas other biomarkers did not differ between groups (p = 0.10-0.66).S100B correlated with BMI (rs = 0.246, p = 0.031) and with age in healthy subjects (rs = 0.345, p = 0.002).Correlation between white matter hyperintensities and NSE underscores the vascular hypothesis of late life depression.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Max Planck Institute for Human Cognitive and Brain Sciences Leipzig, Germany ; University Clinic for Psychiatry and Psychotherapy, Leipzig University Leipzig, Germany ; LIFE-Leipzig Rsearch Center for Civilization Diseases, Leipzig University Leipzig, Germany.

ABSTRACT
Minor depression is diagnosed when a patient suffers from 2 to 4 depressive symptoms for at least 2 weeks. Though minor depression is a widespread phenomenon, its pathophysiology has hardly been studied. To get a first insight into the pathophysiological mechanisms underlying this disorder we assessed serum levels of biomarkers for plasticity, glial and neuronal function: brain-derived neurotrophic factor (BDNF), S100B and neuron specific enolase (NSE). 27 subjects with minor depressive episode and 82 healthy subjects over 60 years of age were selected from the database of the Leipzig population-based study of civilization diseases (LIFE). Serum levels of BDNF, S100B and NSE were compared between groups, and correlated with age, body-mass index (BMI), and degree of white matter hyperintensities (score on Fazekas scale). S100B was significantly increased in males with minor depression in comparison to healthy males, whereas other biomarkers did not differ between groups (p = 0.10-0.66). NSE correlated with Fazekas score in patients with minor depression (rs = 0.436, p = 0.048) and in the whole sample (rs = 0.252, p = 0.019). S100B correlated with BMI (rs = 0.246, p = 0.031) and with age in healthy subjects (rs = 0.345, p = 0.002). Increased S100B in males with minor depression, without alterations in BDNF and NSE, supports the glial hypothesis of depression. Correlation between white matter hyperintensities and NSE underscores the vascular hypothesis of late life depression.

No MeSH data available.


Related in: MedlinePlus

Dot plot for the distribution of serum markers’ levels in healthy males and females (first row), and males and females with minor depression (third row). Median levels of the serum markers are depicted with black horizontal lines. Note that the outlier from the healthy females group is not depicted on the S100B plot. MinD, minor depression; HC, healthy controls; BDNF, brain derived neurotrophic factor; NSE, neuron specific enolase.
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Figure 2: Dot plot for the distribution of serum markers’ levels in healthy males and females (first row), and males and females with minor depression (third row). Median levels of the serum markers are depicted with black horizontal lines. Note that the outlier from the healthy females group is not depicted on the S100B plot. MinD, minor depression; HC, healthy controls; BDNF, brain derived neurotrophic factor; NSE, neuron specific enolase.

Mentions: As depicted in the Figure 2, serum S100B levels were significantly lower in healthy males (0.067 μg/l [0.004]) in comparison with healthy females (0.115 μg/l [0.029]; p = 0.01), whereas there was no sex difference in the minor depression group (male: 0.091 μg/l [0.12]; female: 0.088 μg/l [0.011]; p = 0.53). Removal the abovementioned female outlier did not affect the differences between healthy males and females for S100B. BDNF and NSE did not differ neither between the groups stratified by sex (males p = 0.13–0.95; females p = 0.40–0.42), nor when male and female subjects were compared within the minor depression subgroup (p = 0.10–0.98).


First evidence for glial pathology in late life minor depression: S100B is increased in males with minor depression.

Polyakova M, Sander C, Arelin K, Lampe L, Luck T, Luppa M, Kratzsch J, Hoffmann KT, Riedel-Heller S, Villringer A, Schoenknecht P, Schroeter ML - Front Cell Neurosci (2015)

Dot plot for the distribution of serum markers’ levels in healthy males and females (first row), and males and females with minor depression (third row). Median levels of the serum markers are depicted with black horizontal lines. Note that the outlier from the healthy females group is not depicted on the S100B plot. MinD, minor depression; HC, healthy controls; BDNF, brain derived neurotrophic factor; NSE, neuron specific enolase.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4598479&req=5

Figure 2: Dot plot for the distribution of serum markers’ levels in healthy males and females (first row), and males and females with minor depression (third row). Median levels of the serum markers are depicted with black horizontal lines. Note that the outlier from the healthy females group is not depicted on the S100B plot. MinD, minor depression; HC, healthy controls; BDNF, brain derived neurotrophic factor; NSE, neuron specific enolase.
Mentions: As depicted in the Figure 2, serum S100B levels were significantly lower in healthy males (0.067 μg/l [0.004]) in comparison with healthy females (0.115 μg/l [0.029]; p = 0.01), whereas there was no sex difference in the minor depression group (male: 0.091 μg/l [0.12]; female: 0.088 μg/l [0.011]; p = 0.53). Removal the abovementioned female outlier did not affect the differences between healthy males and females for S100B. BDNF and NSE did not differ neither between the groups stratified by sex (males p = 0.13–0.95; females p = 0.40–0.42), nor when male and female subjects were compared within the minor depression subgroup (p = 0.10–0.98).

Bottom Line: S100B was significantly increased in males with minor depression in comparison to healthy males, whereas other biomarkers did not differ between groups (p = 0.10-0.66).S100B correlated with BMI (rs = 0.246, p = 0.031) and with age in healthy subjects (rs = 0.345, p = 0.002).Correlation between white matter hyperintensities and NSE underscores the vascular hypothesis of late life depression.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Max Planck Institute for Human Cognitive and Brain Sciences Leipzig, Germany ; University Clinic for Psychiatry and Psychotherapy, Leipzig University Leipzig, Germany ; LIFE-Leipzig Rsearch Center for Civilization Diseases, Leipzig University Leipzig, Germany.

ABSTRACT
Minor depression is diagnosed when a patient suffers from 2 to 4 depressive symptoms for at least 2 weeks. Though minor depression is a widespread phenomenon, its pathophysiology has hardly been studied. To get a first insight into the pathophysiological mechanisms underlying this disorder we assessed serum levels of biomarkers for plasticity, glial and neuronal function: brain-derived neurotrophic factor (BDNF), S100B and neuron specific enolase (NSE). 27 subjects with minor depressive episode and 82 healthy subjects over 60 years of age were selected from the database of the Leipzig population-based study of civilization diseases (LIFE). Serum levels of BDNF, S100B and NSE were compared between groups, and correlated with age, body-mass index (BMI), and degree of white matter hyperintensities (score on Fazekas scale). S100B was significantly increased in males with minor depression in comparison to healthy males, whereas other biomarkers did not differ between groups (p = 0.10-0.66). NSE correlated with Fazekas score in patients with minor depression (rs = 0.436, p = 0.048) and in the whole sample (rs = 0.252, p = 0.019). S100B correlated with BMI (rs = 0.246, p = 0.031) and with age in healthy subjects (rs = 0.345, p = 0.002). Increased S100B in males with minor depression, without alterations in BDNF and NSE, supports the glial hypothesis of depression. Correlation between white matter hyperintensities and NSE underscores the vascular hypothesis of late life depression.

No MeSH data available.


Related in: MedlinePlus