ArticleNeurology2026
Dual Dopaminergic and Limbic-Cognitive Contributions to Gait Parameters in De Novo Parkinson Disease.
Article in Neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectivesParkinson disease (PD) is a progressive neurodegenerative disease in which gait impairment is a common and disabling clinical feature. We aimed to characterize the independent and mediated contributions of striatal dopamine transporter (DAT) availability and gray matter (GM) volume to quantitative gait impairment in de novo PD.
methodsIn this prospective study, we consecutively recruited patients with de novo PD fulfilling the UK Brain Bank clinical criteria and healthy controls (HCs) without focal neurologic symptoms and parkinsonism at Wonju Severance Christian Hospital. All participants underwent GAITRite-based gait analysis, and patients further underwent brain MRI for GM volumetry,
resultsA total of 122 patients with de novo PD (mean age, 69.66 years; 45.90% female) and 177 HCs (mean age, 72.07 years; 51.41% female) were enrolled. Compared with HCs, patients with PD showed slower velocity, shorter step/stride lengths, reduced swing and single-support time, increased double-support time, and greater dispersion across multiple gait domains. Limbic-related GM volumes were associated with step/stride lengths and temporal phase composition, and these associations were substantially mediated by global cognition (representative ACMEs [95% CIs] for stride length: posterior cingulate cortex, 1.9559 [0.5606-4.2238]; hippocampus, 3.6722 [1.0707-8.2118]; thalamus, 2.8794 [0.0408-7.2535]; amygdala, 4.9696 [1.8241-10.3405]; proportions mediated, 19%-50%). Lower putaminal DAT availability was associated with greater stance time and double-support time variability, whereas lower caudate DAT availability was associated with longer swing and single-support time and altered phase parameters. These associations were not significantly mediated by bradykinesia/rigidity scores; direct effects remained significant (ADEs [95% CIs]: caudate-swing time, -0.0237 [-0.0428 to -0.0086]; putamen-double-support time variability, -2.0249 [-3.1445 to -0.8835]). DISCUSSION: These findings support a dual-pathway model of gait regulation in patients with de novo PD, where striatal dopaminergic denervation directly affects gait rhythmicity, whereas limbic system atrophy affects gait through direct and cognition-mediated pathways. This medication-naïve cohort may limit generalizability to the broader PD spectrum.
Indexed as
Identifiers
42430674What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.