## 1 Introduction
### Cognitive Decline in Depression  
Although MDD is the most common condition and often has a high recurrence rate, currently used therapeutic approaches do not provide an effective treatment for all those who suffer from it. Depression is a syndrome because it implies a cluster of symptoms and signs that tend to occur together. The two \"basic\" symptoms of depression are a low mood and a loss of interest in activities. In addition, people may experience changes in appetite, sleep problems, fatigue, guilt, difficulty concentrating, thoughts of death, or impaired memory and cognitive function. MDD is associated with structural and functional brain abnormalities that contribute to its debilitating effects, including significant cognitive impairment. MDD includes cognitive dysfunction as a diagnostic criterion, described as a reduced ability to think or concentrate. Other cognitive problems may consist of deficiencies in executive function, problems concentrating and paying attention, learning and memory, and processing speed. Objective assessments of cognitive performance suggest that patients with melancholic depression have a significantly greater degree of impairment in memory and executive function compared with patients with non-melancholic depression. Furthermore, the severity of symptoms, the cumulative duration of depressive episodes, and the presence of comorbidities were all independently and negatively correlated with cognitive function [7]. Research suggests that cognitive deficits are more pronounced in melancholic depression compared to non-melancholic subtypes. Additionally, factors such as symptom severity, cumulative duration of depressive episodes, and comorbid conditions can further exacerbate cognitive decline. The most complex cases require differential diagnosis techniques to distinguish between reversible cognitive impairment related to depression and neurodegenerative conditions such as dementia. However, despite advances in neuroscience, no definitive biomarkers exist for diagnosing MDD or guiding individualized treatment selection. In contrast, despite significant advances in neuroscience, no biomarkers are available to diagnose or identify preferred treatments for people with MDD [8]. Neuroimaging has played a crucial role in enhancing our understanding of the potential neural mechanisms involved in depression, as well as the cognitive impairments observed in depressed individuals. Various morphological, functional, and molecular approaches have been employed to explore these mechanisms. Diffusion Tensor Imaging (DTI) studies using voxel-based morphometry and diffusion tensor imaging showed changes in the anterior cingulate cortex, frontal cortex, island, thalamus, and left longitudinal fasciculus. Abnormal functional connectivity was observed in several brain regions, including the hippocampus, prefrontal white matter, right solitary bundle, corpus callosum, and inferior fronto-occipital bundle. These regions showed altered connectivity within the evidence network (mainly involving the anterior insular cortex and anterior dorsal cingulate cortex) and the cognitive control network (involving the dorsolateral prefrontal cortex and pregenual anterior cingulate cortex). Additionally, there was network hyperactivity observed in the default network (comprising the posterior cingulate, medial prefrontal cortex, precuneus, and temporo-parietal cortex) as well as in the affective network (involving the amygdala, subgenual cingulate, and pregenual cingulate), all of which are associated with cognitive deficits in MDD [8]. Cognitive dysfunction is a key pathological characteristic of MDD, but it is frequently neglected and underappreciated in the diagnosis and treatment of the condition. It significantly influences psychosocial outcomes, including an individual's mental and social well-being and ability to function, which directly impact productivity and the chances of returning to work.