ArticleMovement disorders clinical practice2024
White Matter Abnormalities Track Disease Progression in Multiple System Atrophy.
Article in Movement disorders clinical practice, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Beyond the Wiring: White Matter as a Dynamic Regulator of Brain Function and Disease.Neuroscience bulletin · 2026Review
- Astrocytic FABP5 drives non-cell-autonomous oligodendrocyte injury in multiple system atrophy by promoting TNF signaling and ferroptotic stress.Redox biology · 2026Article
- Multiparametric MRI and imaging transcriptomics reveal molecular and cellular correlates of neurodegeneration in experimental Parkinsonism.NPJ Parkinson's disease · 2026Article
- Precise disease heterogeneity and progression quantification in MSA and Parkinson's disease using machine learning.Scientific reports · 2026Article
- Alpha-Synuclein in Neurodegeneration: From Shared Biology to Disease-Specific Phenotypes.Cells · 2026Review
- Clinical and neuroimaging correlates of disease related gait patterns in patients with multiple system atrophy cerebellar type.Scientific reports · 2025Article
- The MSA Atrophy Index (MSA-AI): An Imaging Marker for Diagnosis and Clinical Progression in Multiple System Atrophy.Annals of clinical and translational neurology · 2025Article
- Trajectories of Pontine Volume in Patients with Multiple System Atrophy.Movement disorders : official journal of the Movement Disorder Society · 2025Article
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Authors and funding
13 authors.
Funding
Abstract
backgroundWhite matter (WM) abnormalities have been implicated in clinically relevant functional decline in multiple system atrophy (MSA).
objectiveTo identify the WM and gray matter (GM) abnormalities in MSA and assess the utility of longitudinal structural and diffusion changes as surrogate markers for tracking disease progression in MSA.
methodsTwenty-seven participants with early MSA [15 with clinically predominant cerebellar (MSA-C) and 12 with clinically predominant parkinsonian features (MSA-P)] and 14 controls were enrolled as a part of our prospective, longitudinal study of synucleinopathies. Using structural magnetic resonance imaging (MRI) and diffusion MRI (diffusion tensor and neurite orientation and dispersion density imaging), we analyzed whole and regional brain changes in these participants. We also evaluated temporal imaging trajectories based on up to three annual follow-up scans and assessed the impact of baseline diagnosis on these imaging biomarkers using mixed-effect models.
resultsMSA patients exhibited more widespread WM changes than GM, particularly in the cerebellum and brainstem, with greater severity in MSA-C. Structural and diffusion measures in the cerebellum WM and brainstem deteriorated with disease progression. Rates of progression of these abnormalities were similar in both MSA subtypes, reflecting increasing overlap of clinical features over time.
conclusionWM abnormalities are core features of MSA disease progression and advance at similar rates in clinical MSA subtypes. Multimodal MRI imaging reveals novel insights into the distribution and pattern of brain abnormalities and their progression in MSA. Selected structural and diffusion measures may be useful for tracking disease progression in MSA clinical trials.
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