中国神经再生研究(英文版) ›› 2024, Vol. 19 ›› Issue (6): 1203-1205.doi: 10.4103/1673-5374.386404

• 观点:退行性病与再生 • 上一篇    下一篇

帕金森病的神经可塑性:神经影像学视角

  

  • 出版日期:2024-06-15 发布日期:2023-11-17

Neural plasticity in Parkinson’s disease: a neuroimaging perspective

Christina Andica*, Koji Kamagata   

  1. Department of Radiology, Juntendo University Graduate School of Medicine, Tokyo, Japan (Andica C, Kamagata K)
    Faculty of Health Data Science, Juntendo University, Chiba, Japan (Andica C)
  • Online:2024-06-15 Published:2023-11-17
  • Contact: Christina Andica, MD, PhD, christina@juntendo.ac.jp.
  • Supported by:
    This work was partially supported by the Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research (KAKENHI; Grant numbers 23H02865 [to KK], 23K14927 [to CA]), the Brain/MINDS Beyond program of the Japan Agency for Medical Research and Development (Grant Number JP19dm0307101 [to KK]).

摘要: https://orcid.org/0000-0002-9339-6950 (Christina Andica)

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.