ArticleScientific reports2025
Characterization of lower urinary tract dysfunction in a mouse model of amyotrophic lateral sclerosis.
Article in Scientific reports, 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.
- Intravenous administration of an engineered AAV9-gene-silencing vector suppresses human SOD1 and extends survival in an ALS mouse model.Nature communications · 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
Amyotrophic lateral sclerosis (ALS) is characterized by a progressive loss of motor function due to degeneration of motor neurons. In addition to motor-related symptoms, increasing evidence from clinical studies indicate lower urinary tract (LUT) dysfunctions (urge incontinence) are found in patients with ALS, which causes a significant negative impact on quality of life. However, it remains unclear whether LUT dysfunction can be validated in preclinical ALS models. Here, we attempt to answer this question by using comprehensive urodynamic testing with electromyogram of external urethral sphincter (EUS) activity in both female and male SOD1-G93A ALS mice at both 9 weeks of age (pre-onset stage) and 16 weeks of age (early symptomatic stage). Our results demonstrate that the detrusor muscle is hyperactive, voiding volume is decreased, and the EUS relaxation period is shorter in female and male SOD1-G93A ALS mice at both 9 weeks and 16 weeks of age, compared to age-matched wild-type animals. The symptoms of urge incontinence found in the current study are similar to the clinical findings, indicating that SOD1-G93A ALS mice can be used as a preclinical model to develop therapeutics for ALS patients with LUT dysfunction.
Indexed as
Identifiers
What Socratic 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 Socratic graph.