Abstract: Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized primarily by classical motor signs of bradykinesia, rigidity, tremors, and postural instability usually manifesting unilaterally or at least asymmetrically. The disease involves a loss of dopaminergic neurons projecting from the substantia nigra pars compacta to the dorsal striatum, and the presence of Lewy bodies and Lewy neurites (intraneuronal inclusions composed of misfolded and aggregated α-synuclein; Tagliaferro and Burke, 2016). Literature suggests that PD symptoms appear only after a substantial loss of dopaminergic neurons, i.e., around 50–70% of striatal dopaminergic terminals and 30% of substantia nigra dopaminergic neurons (Tagliaferro and Burke, 2016). Several PD subtypes based on the presentation, such as the tremor-dominant (TD) type and PD with right-side dominant symptoms, have been found to demonstrate a better prognosis and a less severe clinical picture than PD-related postural instability and gait disorders and left-dominant PD, respectively. In this regard, the neuronal compensatory response is considered responsible for delaying or reducing the severity of PD-related symptoms. Furthermore, histopathological research conducted on the brain tissues of PD mice models, which express the A53T mutation in the α-synuclein gene, demonstrated increased axonal arborization and collateralization in the white matter (Schechter et al., 2020). These findings suggest that α-synuclein is essential in promoting axonal growth during the early stages of the disease (Schechter et al., 2020). Similarly, studies involving brain tissues of human PD patients showed adaptive changes in motor circuits within the brain characterized by axonal collateralization, as well as an increase in the size and density of oligodendrocytes (Fu et al., 2022). Therefore, expanding our knowledge of neuroplasticity within the cortical-basal ganglia-thalamocortical circuits may have valuable implications in the development of innovative therapies and early-stage diagnostic approaches for PD. However, the current literature on PD does not adequately address the evidence regarding neural plasticity, presumably because of the limitations of in vivo imaging techniques in accurately capturing microstructural changes in brain tissue. This perspective article aimed to outline the utilization of advanced magnetic resonance imaging (MRI) techniques, including diffusion MRI and myelin imaging, to assess the microstructure of brain tissue to elucidate neural plasticity in Parkinson’s disease. Furthermore, the article explored potential future prospects in this field.