## 4 Discussion  
The present findings confirm the previously postulated hypothesis: as the depression group was the only group affected by the tDCS protocol, it suggests that the participants' baseline characteristics drive their cortical hemodynamic response to tDCS. The baseline minimum rates of SatO\({}_{2}\), along with the minimum HbO values, were significantly lower in the depression group compared to the control group. Additionally, after the protocol, only the depression group showed increased levels of minimal SatO\({}_{2}\), while the control group's SatO\({}_{2}\) and HbO responses remained unchanged during the intervention, with a relevant positive trend for the depression group. Using minimum, maximum, and mean values of brain oxygen saturation in fNIRS analysis provides a more comprehensive understanding of the brain's oxygenation status. The mean values offer a general indication of the brain's overall oxygenation status and can be useful for identifying baseline oxygen levels or changes due to an intervention. However, the minimum rates can help identify periods of potential hypoxia or critical low points that could indicate issues such as impaired blood flow, metabolic demand exceeding supply, or other pathological conditions. Understanding the minimum oxygenation level is crucial for assessing the safety and potential risks to brain health. On the other hand, maximum rates are able to highlight periods of hyperoxia or peak oxygenation. This information is valuable for understanding the upper limits of oxygenation and ensuring that they are within safe physiological ranges. It can also indicate the brain's capacity to increase oxygen supply when needed [17,21]. The present study reinforces the idea that anodal stimulation may increase the cortex hemodynamic response. An fMRI-based study showed that a range of anodal intensities applied over the primary motor cortex increased the cerebral blood flow under the electrode, with 2 mA increasing the greatest (15.3%) compared to sham controls [22]. In fact, pre-clinical studies have already shown that both vasodilation and increased blood flow \begin{table}
\begin{tabular}{c c c c c c c c c} \hline \hline \multirow{3}{*}{\begin{tabular}{c} **Outcome** \\ **(g/dL)** \\ \end{tabular} } & \multicolumn{2}{c}{\begin{tabular}{c} **Depression Group (\(n\) = 16)** \\ **Mean \(\pm\) SD** \\ \end{tabular} } & \multirow{3}{*}{\begin{tabular}{c} **Within-** \\ **Group** \\ **Differences** \\ \end{tabular} } & \multicolumn{2}{c}{\begin{tabular}{c} **Control Group (\(n\) = 16)** \\ **Mean \(\pm\) SD** \\ \end{tabular} } & \multirow{3}{*}{\begin{tabular}{c} **Within-** \\ **Group** \\ **Differences** \\ \end{tabular} } & \multicolumn{2}{c}{\begin{tabular}{c} **Between-Group** \\ **Differences** \\ **Baseline** \\ \end{tabular} } \\ \cline{2-2} \cline{4-10}  & **Baseline** & \begin{tabular}{c} **Post-** \\ **Stimulation** \\ \end{tabular} & & & **Baseline** & \
\begin{tabular}{c} **Post-** \\ **Stimulation** \\ \end{tabular} & & & **Baseline** &
\begin{tabular}{c} **Post-** \\ **Stimulation** \\ \end{tabular} \\ \hline Mean & 5.94 \(\pm\) 0.97 & 6.29 \(\pm\) 1.35 & ns & 6.76 \(\pm\) 0.75 & 6.84 \(\pm\) 0.76 & ns & ns & ns \\ Minimum & 5.25 \(\pm\) 1.74 & 6.04 \(\pm\) 1.43 & 0.002 * & 6.54 \(\pm\) 0.72 & 6.64 \(\pm\) 0.86 & ns & 0.04 * & ns \\ Maximum & 6.39 \(\pm\) 0.96 & 6.55 \(\pm\) 1.35 & ns & 6.94 \(\pm\) 0.78 & 6.93 \(\pm\) 0.77 & ns & ns & ns \\ \hline \hline \end{tabular}  
* Significant difference assigned. Legend: ns = non-significant.  
\end{table} 
Table 3: Comparison of HbO levels between and within groups. Figure 2: Oxygen saturation (SatO\({}_{2}\)) group trends with regression equations. Legend: DG = depression group; CG = control group. could be the primary responses of the vessels to tDCS [14; 23]. The increase in neuronal resting membrane potentials could be then a secondary response, along with the increased likelihood of neuron depolarization.