ArticleScientific reports2019
Traumatic Brain Injury-related voiding dysfunction in mice is caused by damage to rostral pathways, altering inputs to the reflex pathways.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- Mouse closed head traumatic brain injury replicates the histological tau pathology pattern of human disease: characterization of a novel model and systematic review of the literature.Acta neuropathologica communications · 2021Pooled it
- Efficacy of expanded periurethral cleansing in reducing catheter-associated urinary tract infection in comatose patients: a randomized controlled clinical trial.Critical care (London, England) · 2024Trial
- The cerebro-pelvic axis: a unified framework linking higher brain function, pelvic floor control, and lower urinary tract dysfunction.Frontiers in neuroscience · 2026Article
- Meningeal lymphatic architecture and drainage dynamics surrounding the human middle meningeal artery.iScience · 2025Article
- The glymphatic and meningeal lymphatic systems may converge, connecting traumatic brain injury progression with chronic traumatic encephalopathy onset.Molecular and cellular neurosciences · 2025Review
- Immunization targeting diseased proteins in synucleinopathy and tauopathy: insights from clinical trials.Translational neurodegeneration · 2025Review
- ML-UrineQuant: A machine learning program for identifying and quantifying mouse urine on absorbent paper.Physiological reports · 2025Article
- Pin1-catalyzed conformational regulation after phosphorylation: A distinct checkpoint in cell signaling and drug discovery.Science signaling · 2024Review
- Review
- p17/C18-ceramide-mediated mitophagy is an endogenous neuroprotective response in preclinical and clinical brain injury.PNAS nexus · 2024Article
- The role of the Pin1-Frontiers in cell and developmental biology · 2024Review
- Catheter-Associated Urinary Tract Infection (CAUTI) in the NeuroICU: Identification of Risk Factors and Time-to-CAUTI Using a Case-Control Design.Neurocritical care · 2021Article
- Chronic traumatic encephalopathy-a blueprint for the bridge between neurological and psychiatric disorders.Translational psychiatry · 2020Review
- Managing Acute Urinary Dysfunction for Neurologic Injury Patients.Journal of experimental neurology · 2020Article
- Cystometric Measurements in Rats with an Experimentally Induced Traumatic Brain Injury and Voiding Dysfunction: A Time-Course Study.Brain sciences · 2019Article
- Pathogenesis evidence from human and animal models of detrusor underactivity.Tzu chi medical journalReview
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
Abstract
Brain degeneration, including that caused by traumatic brain injury (TBI) often leads to severe bladder dysfunction, including incontinence and lower urinary tract symptoms; with the causes remaining unknown. Male C57BL/6J mice underwent repetitive moderate brain injury (rmdTBI) or sham injury, then mice received either cis P-tau monoclonal antibody (cis mAb), which prevents brain degeneration in TBI mice, or control (IgG). Void spot assays revealed age-dependent incontinence in IgG controls 8 months after injury, while cis mAb treated or sham mice showed no dysfunction. No obvious bladder pathology occurred in any group. Urodynamic cystometry in conscious mice revealed overactive bladder, reduced maximal voiding pressures and incontinence in IgG control, but not sham or cis mAb treated mice. Hyperphosphorylated tau deposition and neural tangle-like pathology occurred in cortical and hippocampal regions only of IgG control mice accompanied with post-traumatic neuroinflammation and was not seen in midbrain and hindbrain regions associated with bladder filling and voiding reflex arcs. In this model of brain degeneration bladder dysfunction results from rostral, and not hindbrain damage, indicating that rostral brain inputs are required for normal bladder functioning. Detailed analysis of the functioning of neural circuits controlling bladder function in TBI should lead to insights into how brain degeneration leads to bladder dysfunction, as well as novel strategies to treat these disorders.
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Registered trials
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