ArticleGeroScience2026
Subcortical white matter hyperintensities and motor function in parkinson's disease: findings from the ONDRI study.
Article in GeroScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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20 authors.
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Abstract
backgroundMotor signs, such as rigidity, bradykinesia, tremor, gait and balance impairment, are hallmark features of idiopathic Parkinson's disease (PD). The basal ganglia, involved in voluntary and automatic movements, are affected by reduced dopaminergic activity, contributing to motor signs in PD. Motor signs may be exacerbated by cortical white matter hyperintensities (WMH), but the relationship between basal ganglia WMH and motor signs remains unclear.
objectiveTo investigate the association between subcortical WMH burden and motor severity in PD participants.
methodThis cross-sectional study included 140 PD participants from the Ontario Neurodegenerative Disease Research Initiative (ONDRI). The relative WMH (i.e, percentage) in the whole brain, frontal, temporal, parietal, occipital lobes, and basal ganglia+thalamus (BGT) were calculated. Adjusted regression models were used to test the associations between WMH and motor signs. WMH burden was stratified by quartiles, and Analysis of Covariance was applied to determine which WMH quartile most affected motor signs.
resultsIncreased WMH burden in BGT was associated with better motor function. In contrast, WMH burden in cortical brain regions, i.e., frontal, parietal, temporal, and occipital lobes, was not associated with worse motor signs. Participants with larger BGT WMH volumes exhibited better motor function compared to those in lower quartiles
conclusionHyperintense lesions in the basal ganglia+thalamus were significantly associated with better motor function, suggesting that disruption of inhibitory basal ganglia circuitry may recalibrate motor output. These findings raise novel hypotheses about circuit-level modulation in Parkinson's disease and may guide future mechanistic and therapeutic investigations. However, as the results are correlational, they do not imply causality.
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