## 4 Discussion
The hypothesis that the direct influence of thalamic dopamine from the SNc may modulate large-scale thalamo-cortical networks could provide a theoretical framework for explaining some non-motor symptoms in PD and other neuropsychiatric conditions. Research by [PERSON] et al. (2014) [79] highlighted that the SN has a dual role in influencing thalamic activity through both inhibitory and excitatory outputs. This dual mechanism suggests a complex synaptic connection that allows the basal ganglia to modulate thalamic activity in a subtle manner, which is essential for various motor and cognitive functions. A study by [PERSON] et al. (2020) utilizing ex vivo diffusion tensor imaging and tractography identified fiber connections between the substantia nigra and thalamus within the human subthalamic area, to map these pathways [80]. The significance of this direct pathway remains to be fully elucidated; however, its existence serves to reinforce the role of the SN as a central integrator of both motor and cognitive functions, as well as sensory functions. The evidence reviewed above illustrates that distinct components of the SN network are selectively affected in different pathological conditions, with specific disruptions correlating with clinical symptoms. For instance, degeneration of the nigrostriatal pathway is closely linked to the motor deficits of PD [12; 62; 70], whereas reduced connectivity between the SN and globus pallidus or limbic structures has been observed in patients with MDD and addiction [67; 69; 75]. Altered connectivity between the SN and the thalamus or prefrontal cortex may further contribute to cognitive dysfunction and impulsivity [69; 73]. In this context, structural connectivity mapping of SN circuits may hold promise for advancing individualized diagnostic and therapeutic strategies. Subject-specific tractography can identify patterns of circuit disruption that underlie motor, affective, or cognitive impairments, potentially guiding personalized interventions. For instance, mapping the integrity of pathways such as the medial forebrain bundle or SN and thalamus projections may inform deep brain stimulation target selection or stratify patients for pharmacological therapies. Integrating diffusion imaging with genetic, behavioral, and clinical markers may further enhance the precision of diagnosis and treatment planning in disorders involving SN dysfunction [67; 78]. Building on this expanded network view, the imaging of SN connectivity using advanced tractography represents a promising tool not only for research but potentially for clinical practice. In addition to its association with PD, there is an emerging body of evidence that suggests these pathways may also play a role in a wide range of neuropsychiatric conditions. Future research should aim to validate the use of connectivity markers against longitudinal data, integrating structural and functional methods, and further subdividing individual SN subregions. It is imperative that particular emphasis is placed on the standardization of methodology and the development of applications in the field of personalized medicine. Considering the complex connectivity of the SN and its role in various pathologies, it is important to take into account additional brain regions that may act as potential nodes within SN-related networks. One such structure is the zona incerta (ZI), a subthalamic area that has attracted increasing interest due to its anatomical and functional connections with components of the SN [81; 82]. [PERSON] et al. (2020) [83] reported, based on both preclinical findings and therapeutic outcomes in humans, that the ZI maintains widespread anatomical connectivity with the SNr and SNc. They suggested that deep brain stimulation targeting the ZI may exert its therapeutic effects in [PERSON]'s disease by restoring the function of a broader SN-ZI-thalamus-striatum network. Supporting this notion, recent findings by [PERSON] et al.