ArticleDystonia (Lausanne, Switzerland)2025
Altered Functional Brain Connectivity in Dyt1 Knock-in mouse models.
Article in Dystonia (Lausanne, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Emotion-tremor coupling in Wilson's disease: EEG microstate C as a marker of salience network dysregulation.Orphanet journal of rare diseases · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
DYT1 dystonia is an early onset, generalized form of isolated dystonia characterized by sustained involuntary muscle co-contraction, leading to abnormal movements and postures. It is the most common hereditary form of primary dystonia, caused by a trinucleotide GAG deletion in the DYT1 gene, which encodes the TorsinA protein. Recent studies conceptualized dystonia as a functional network disorder involving basal ganglia, thalamus, cortex and cerebellum. However, how TorsinA dysfunction in specific cell types affects network connectivity and dystonia-related pathophysiology remains unclear. In this study, we aimed to elucidate the impact of the GAG TorsinA mutation present globally and when restricted to the cortical and hippocampal neurons. To accomplish this, we generated two distinct Dyt1 mouse models, one with Dyt1 dGAG knock-in throughout the body (dGAG) and another with a cerebral cortex-specific Dyt1 dGAG knock-in using Emx1 promoter (EMX). In both models, we performed
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.