ArticleMovement disorders : official journal of the Movement Disorder Society2013
Bladder dysfunction in a transgenic mouse model of multiple system atrophy.
Article in Movement disorders : official journal of the Movement Disorder Society, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 67 citations in OpenAlex.
- MMP-2 Responsive Functional Bladder Acellular Matrix Scaffold Combined With Urine Derived Stem Cells for Bladder Nerve Regeneration.Chembiochem : a European journal of chemical biology · 2026Article
- Multiparametric MRI and imaging transcriptomics reveal molecular and cellular correlates of neurodegeneration in experimental Parkinsonism.NPJ Parkinson's disease · 2026Article
- Transcriptional dysregulation in the cerebellum triggered by oligodendroglial α-synucleinopathy: insights from a transgenic mouse into the early disease mechanisms of MSA.Journal of neural transmission (Vienna, Austria : 1996) · 2026Article
- Review
- Multiple system atrophy related neurogenic bladder: mechanism and treatment.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Review
- A novel mouse model for investigating α-synuclein aggregates in oligodendrocytes: implications for the glial cytoplasmic inclusions in multiple system atrophy.Molecular brain · 2024Article
- A Mouse Model of Multiple System Atrophy: Bench to Bedside.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Female Urinary Retention Progressing to Possible Multiple System Atrophy-cerebellar Form after 12 Years.Internal medicine (Tokyo, Japan) · 2022Article
- The Compound ATH434 Prevents Alpha-Synuclein Toxicity in a Murine Model of Multiple System Atrophy.Journal of Parkinson's disease · 2022Article
- A historical review of multiple system atrophy with a critical appraisal of cellular and animal models.Journal of neural transmission (Vienna, Austria : 1996) · 2021Review
- Article
- Propagation of Pathological α-Synuclein from the Urogenital Tract to the Brain Initiates MSA-like Syndrome.iScience · 2020Article
- Assessment of the Retina of Plp-α-Syn Mice as a Model for Studying Synuclein-Dependent Diseases.Investigative ophthalmology & visual science · 2020Article
- High-salt diet does not boost neuroinflammation and neurodegeneration in a model of α-synucleinopathy.Journal of neuroinflammation · 2020Article
- Models of multiple system atrophy.Experimental & molecular medicine · 2019Review
- Article
- Anle138b modulates α-synuclein oligomerization and prevents motor decline and neurodegeneration in a mouse model of multiple system atrophy.Movement disorders : official journal of the Movement Disorder Society · 2019Article
- Parkinsonian GM2 synthase knockout mice lacking mature gangliosides develop urinary dysfunction and neurogenic bladder.Experimental neurology · 2019Article
- In vitro models of multiple system atrophy from primary cells to induced pluripotent stem cells.Journal of cellular and molecular medicine · 2018Review
- Progressive striatonigral degeneration in a transgenic mouse model of multiple system atrophy: translational implications for interventional therapies.Acta neuropathologica communications · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Multiple system atrophy (MSA) is an adult-onset neurodegenerative disorder presenting with motor impairment and autonomic dysfunction. Urological function is altered in the majority of MSA patients, and urological symptoms often precede the motor syndrome. To date, bladder function and structure have never been investigated in MSA models. We aimed to test bladder function in a transgenic MSA mouse featuring oligodendroglial α-synucleinopathy and define its applicability as a preclinical model to study urological failure in MSA. Experiments were performed in proteolipid protein (PLP)-human α-synuclein (hαSyn) transgenic and control wild-type mice. Diuresis, urodynamics, and detrusor strip contractility were assessed to characterize the urological phenotype. Bladder morphology and neuropathology of the lumbosacral intermediolateral column and the pontine micturition center (PMC) were analyzed in young and aged mice. Urodynamic analysis revealed a less efficient and unstable bladder in MSA mice with increased voiding contraction amplitude, higher frequency of nonvoiding contractions, and increased postvoid residual volume. MSA mice bladder walls showed early detrusor hypertrophy and age-related urothelium hypertrophy. Transgenic hαSyn expression was detected in Schwann cells ensheathing the local nerve fibers in the lamina propria and muscularis of MSA bladders. Early loss of parasympathetic outflow neurons and delayed degeneration of the PMC accompanied the urological deficits in MSA mice. PLP-hαSyn mice recapitulate major urological symptoms of human MSA that may be linked to αSyn-related central and peripheral neuropathology and can be further used as a preclinical model to decipher pathomechanisms of MSA.
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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 OpenQuestion graph.