## 4 Discussion
It has been hypothesized that alterations in the connectivity of these circuits may affect the transmission of inhibitory signals to the thalamus and subsequently to the cortex, with the potential to affect motor output [7,34]. The results of this study underscore the significance of tractographic imaging not only of classical pathways but also of output connections, which may serve as a target for therapeutic intervention in a range of motor disorders. [PERSON] et al. (2023) [78] explored the microstructural changes in the SN and its tracts to the dorsal striatum and dorsolateral prefrontal cortex in PD patients using diffusion MRI and histopathology. The research involved post-mortem analysis of PD and control donors, revealing increased MD and FA in specific SN tracts in PD compared to controls. These microstructural alterations were associated with dopaminergic degeneration and Lewy neurite pathology, suggesting that diffusion MRI can effectively capture these changes and potentially aid in understanding motor and cognitive impairments in these disorders. In addition to motor function, the SN also affects a range of behavioral and cognitive functions, as evidenced by impulsivity disorders, addictions, and mood disorders. Impulsivity manifests in diverse forms within the context of the basal ganglia, encompassing motor impulsiveness, characterized by an inability to inhibit action, and decision-making impulsivity, marked by a propensity to seek reward irrespective of risk. A review of the extant literature confirms that dopaminergic inputs from the SN/VTA to limbic and prefrontal regions are significantly involved in modulating memory, learning, and impulsivity [66]. Research by [PERSON] et al. (2022) [67] demonstrated that structural connectivity between the SN/VTA and the hippocampus is associated with the capacity for memory concerning motivation (e.g., potential reward). Therefore, the SN is hypothesized to function as a central node in the modulation of motivated behavior and learning. Recent research by [PERSON] et al. (2024) [75] utilizing 7T DTI revealed a substantial decrease in connectivity between the SN and GP in patients diagnosed with major depressive disorder (MDD). It is hypothesized that this pathway constitutes a motor component of the BG output system; however, its disruption in MDD suggests the possibility of a regulatory role in motivation, reward, and emotional state. Correlations with insomnia scores and age of onset provide further evidence for the functional importance of this pathway in non-motor symptoms of affective disorders. Dopaminergic projections from the SN/VTA to the ventral striatum have been demonstrated to play a critical role in the regulation of impulsivity and motivated behavior. The research conducted by [PERSON] et al. (2020) [69] and [PERSON] et al. (2023) [73] demonstrated a robust correlation between the structural integrity of these pathways (e.g., the medial forebrain bundle) and measures of impulsiveness. The study further suggested that these pathways can be subject to developmental modulation by genetic factors, such as polymorphisms in the FTO. It has been demonstrated that individuals with higher levels of motor impulsivity, and patients diagnosed with stimulant use disorder, exhibit increased levels of connectivity within these circuits. This finding serves to substantiate their significance in the context of the neurobiology of addiction and behavioral disorders. This provides a novel basis for research, establishing a link between neurodevelopment, genetics, and imaging with a view to comprehend the brain circuits underpinning behavior. The identification of the direct dopaminergic SNc-thalamus pathway [28] offers novel insights into the non-motor symptoms of PD, including hallucinations, REM sleep disturbances, and cognitive dysfunction.