Dose-dependent effects of transcranial photobiomodulation on brain temperature in patients with major depressive disorder: a spectroscopy study.

This study aimed to evaluate the dose-dependent brain temperature effects of transcranial photobiomodulation (t-PBM). Thirty adult subjects with major depressive disorder were randomized to three t-PBM sessions with different doses (low: 50 mW/cm2, medium: 300 mW/cm2, high: 850 mW/cm2) and a sham treatment. The low and medium doses were administered in continuous wave mode, while the high dose was administered in pulsed wave mode. A 3T MRI scanner was used to perform proton magnetic resonance spectroscopy (1H-MRS). A voxel with a volume of 30 × 30 × 15 mm3 was placed on the left prefrontal region. Brain temperature (°C) was derived by analyzing 1H-MRS spectrum chemical shift differences between the water (~ 4.7 ppm) and N-acetyl aspartate (NAA) (~ 2.01 ppm) peaks. After quality control of the data, the following group numbers were available for both pre- and post-temperature estimations: sham (n = 10), low (n = 11), medium (n = 10), and high (n = 8). We did not detect significant temperature differences for any t-PBM-active or sham groups post-irradiation (p-value range = 0.105 and 0.781). We also tested for potential differences in the pre-post variability of brain temperature in each group. As for t-PBM active groups, the lowest fluctuation (variance) was observed for the medium dose (σ2 = 0.29), followed by the low dose (σ2 = 0.47), and the highest fluctuation was for the high dose (σ2 = 0.67). t-PBM sham condition showed the overall lowest fluctuation (σ2 = 0.11). Our 1H-MRS thermometry results showed no significant brain temperature elevations during t-PBM administration.

Plasma Neuronal and Glial Markers and Anterior Cingulate Metabolite Levels in Major Depressive Disorder: A Pilot Study.

INTRODUCTION: Neuroglial functions may be deteriorated in major depressive disorder (MDD). OBJECTIVE: To evaluate the markers of glial and neuronal cell turnover and to explore their associations with brain metabolites. METHODS: In 10 participants with MDD and 10 healthy controls (HC) we investigated neuronal and glial plasma markers (the neuron-specific enolase, NSE; and S100beta, S100B) and brain metabolites (N-acetyl aspartate, NAA; total choline, Cho; and total creatine, Cr). Blood was collected for NSE and S100B. NAA, Cho, and Cr metabolite levels were measured in the anterior cingulate cortex (ACC) with proton magnetic resonance spectroscopy (1H-MRS) at 3T. RESULTS: NSE and S100B levels were significantly higher in MDD subjects than in HC. The Cr level was significantly higher in MDD subjects than in HC, but the NAA and Cho levels did not differ between groups. NAA/Cr and Cho/Cr ratios were significantly lower in patients with MDD versus HC. S100B was negatively correlated with the Cho levels. CONCLUSIONS: These results provide supporting evidence of neuronal and glial distress in MDD. Neuronal viability appears decreased, whereas glial regenerative activity and energy metabolism in the ACC increase in acute major depressive episode. Since low concentrations of S100B have neuroplastic effects, these changes may indicate a possible compensatory mechanism.

Correlation between S100B and severity of depression in MDD: A meta-analysis.

BACKGROUND: Previous studies have demonstrated elevated levels of the S100B protein (located in glial cells) in major depressive disorder (MDD) as compared to healthy controls. However, studies reporting correlation between S100B levels and depression severity have been conflicting. METHODS: We investigated, through systematic review and meta-analysis, whether the correlation between S100B levels and depression severity is significant in patients with MDD. Pearson correlation coefficients reported in the individual studies were converted to Fisher's Z scores, then pooled using the random effects model. Meta-regression was used to test modifiers of the effect size. RESULTS: Sixteen studies including 658 patients with MDD met eligibility criteria. No publication bias was observed. There was a significant and positive correlation between serum S100B level and depression severity (r = 0.204, z = 2.297, p = 0.022). A meta-regression determined that onset age of MDD and percentage of female participants are significant modifiers of this correlation. A moderate, but non-significant heterogeneity was observed in serum studies (44%). CONCLUSION: As many studies have reported significantly increased levels of S100B in MDD compared to controls, this meta-analysis supports the assumption that the increase in S100B correlates with the severity of MDD. Additional studies investigating the precise biological connection between S100B and MDD are indicated.

Electroencephalography-derived biomarkers of antidepressant response.

Recent meta-analyses point to the relatively low efficacy of commonly used antidepressant medications. Selecting the most effective medications for depressed subjects having failed previous treatments is especially difficult. There is a clear need for objective biomarkers that could assist and optimize such treatment selection. We will review here a growing body of evidence suggesting that several electroencephalography (EEG)-based methods may be useful for predicting antidepressant response and eventually for guiding clinical treatment decisions. While most of these methods are based on resting-state EEGs (e.g., alpha- and theta-band EEG abnormalities, the combined Antidepressant Response Index (ATR), cordance, referenced EEG), others include EEG source localization and evoked potentials. The limitations of these technologies and the potential clinical uses will also be outlined.