ArticleMovement disorders : official journal of the Movement Disorder Society2026
In Vivo Mapping of Catecholaminergic Loss and Iron Deposition in Huntington's Disease.
Article in Movement disorders : official journal of the Movement Disorder Society, 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
12 authors.
Funding
Abstract
backgroundThe pathophysiology of Huntington's disease (HD) remains obscure. Magnetic resonance imaging (MRI) can reveal in vivo molecular changes related to disease pathology.
objectivesTo investigate catecholaminergic neuronal integrity and subcortical brain iron accumulation in HD employing neuromelanin-sensitive MRI, and quantitative susceptibility mapping (QSM-MRI).
methodsTwenty-five HD gene expansion carriers (HDGECs; 11 premanifest, mean predicted phenoconversion time 21.25 ± 8.28 years) and 25 healthy controls (HC) underwent clinical investigation, measurement of plasma neurofilament light chain (NfL) levels, neuromelanin-sensitive, and QSM-MRI on a 3 T scanner. For neuromelanin analysis, the substantia nigra (SN) and locus coeruleus (LC) areas and contrast-to-noise ratio (CNR) were computed. Regions of interest from the MuSus100 atlas were segmented for QSM-MRI analysis, and susceptibility values extracted using the whole brain mask as reference.
resultsManifest HDGECs showed, on neuromelanin-sensitive MRI analysis, reduced LC and SN areas, and LC CNR compared with HC (P < 0.001). QSM analysis demonstrated increased susceptibility values in caudate, putamen, external and internal pallidum, and the subthalamic nucleus of manifest HGDECs (P < 0.001). Higher susceptibility values in these regions correlated with clinical markers of disease burden, higher plasma NfL, and poorer neuropsychological outcomes in multiple domains (P < 0.05). Smaller LC area correlated with higher plasma NfL (P = 0.029). Higher susceptibility values in the caudate and putamen correlated with lower SN CNR (P < 0.05).
conclusionsOur findings confirm widespread iron subcortical accumulation in HD, reveal significant noradrenergic neuronal loss, and describe dopaminergic alteration which may reflect ongoing pathology along the nigrostriatal pathway. © 2026 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.
Indexed as
Identifiers
What 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.