ArticleNature communications2025
Cell-specific mechanisms drive connectivity across the time course of Huntington's disease.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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.
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Who cites it
3 citing papers in PubMed.
- The genetic architecture of cortical similarity networks.Nature communications · 2026Article
- Large scale functional and effective connectivity alterations cross the Huntington's disease integrated staging system.NeuroImage. Clinical · 2026Article
- Investigation of cerebral cortical morphological similarity and network topological abnormalities in hepatic encephalopathy utilizing a morphometric inverse divergence network framework.Frontiers in neurologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors.
Funding
Abstract
Hyperconnectivity in functional brain networks occurs decades before disease onset in Huntington's disease. However, the biological mechanisms remain unknown. We investigate connectivity in Huntington's disease using Morphometric INverse Divergence (MIND) in three Huntington's disease cohorts (N = 512) spanning from two decades before the onset of symptoms through to functional decline. Here, we identify stage-specific profiles, with hyperconnectivity 22 years from predicted motor onset, progressing to hypoconnectivity through the late premanifest and manifest stages, showing that hypoconnectivity is correlated with neurofilament light concentrations. To understand the biological mechanisms, we investigate associations with cortical organization principles including disease epicentres and cell-autonomous systems, in particular neurotransmitter distribution. The contribution from disease epicentres is limited to late premanifest while cell-autonomous associations are demonstrated across the Huntington's disease lifespan. Specific relationships to cholinergic and serotoninergic systems localized to granular and infragranular cortical layers are identified, consistent with serotoninergic layer 5a neuronal vulnerability previously identified in post-mortem brains.
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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 Socratic graph.