ArticleJournal of Parkinson's disease2024
Atrophy-related corticospinal changes in advanced Parkinson's disease are associated with the genetic etiology of the disease.
Article in Journal of Parkinson's disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- A narrative review of motor control dual pathways: the corticospinal and reticulospinal tracts in synergy and differentiation.Frontiers in neuroanatomy · 2026Review
- Inherent variability limits clinical utility of reproducible Parkinson's transcriptomics signatures.NPJ Parkinson's disease · 2025Article
- Cerebral microstructural alteration patterns in motor subtypes of Parkinson's disease: a neurite orientation dispersion and density imaging study.Quantitative imaging in medicine and surgery · 2025Article
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Authors and funding
9 authors.
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Abstract
backgroundCompensatory mechanisms in Parkinson's disease (PD) are thought to explain the temporal delay between the beginning of the neurodegenerative process and the appearance of clinical signs. The enhanced structural integrity of the corticospinal tract was previously suggested as one of these mechanisms.
objectiveTo understand the relations between corticospinal tract integrity and the anatomical, clinical, electrophysiological, and genetic PD characteristics.
methodsWe analyzed diffusion tensor imaging (DTI) fractional anisotropy (FA) data from 40 genotyped patients with PD (18 without known genetic cause, 11 with
resultsPD is associated with higher corticospinal FA values (p < 0.001) that are negatively correlated with the disease duration (p = 0.032), confirming previous results. Higher FA values are negatively correlated with cerebral grey matter volumes (p < 0.001) but not with the motor or cognitive PD characteristics, or with the subthalamic beta-oscillatory activity measured intra-operatively. Increased corticospinal FA values are strongly affected by the genetic etiology of PD, with higher values in the monogenic forms of the disease (p < 0.001). The compensatory index, calculated by dividing the corticostriatal FA value by the cerebral grey matter volume, is highest in
conclusionsThe genetic etiology of PD strongly shapes corticospinal tract changes along with disease-duration and cerebral grey matter atrophy. The changes may serve as compensatory mechanism.
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