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Mouse Bladder Wall Injection
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Bladder dysfunction in a transgenic mouse model of multiple system atrophy.

Mathieu Boudes1, Pieter Uvin, Silvia Pinto

  • 1Laboratory of Biomarkers, Screening and Diagnosis, Department of Development and Regeneration, KU Leuven, Leuven, Belgium.

Movement Disorders : Official Journal of the Movement Disorder Society
|February 22, 2013
PubMed
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Multiple system atrophy (MSA) causes bladder dysfunction due to α-synucleinopathy. This study shows a transgenic mouse model exhibits key urological symptoms, aiding research into MSA neurodegeneration.

Area of Science:

  • Neuroscience
  • Urology
  • Pathology

Background:

  • Multiple system atrophy (MSA) is a neurodegenerative disease affecting motor and autonomic functions.
  • Urological dysfunction is common in MSA, often preceding other symptoms.
  • No existing MSA models have investigated bladder function or structure.

Purpose of the Study:

  • To evaluate bladder function in a transgenic mouse model of MSA.
  • To determine the utility of this model for studying urological failure in MSA.
  • To investigate the underlying neuropathology in the bladder and central nervous system.

Main Methods:

  • Assessment of diuresis, urodynamics, and detrusor muscle contractility in proteolipid protein (PLP)-human α-synuclein (hαSyn) transgenic mice and controls.
  • Analysis of bladder morphology and neuropathology in the lumbosacral intermediolateral column and pontine micturition center (PMC).

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  • Detection of hαSyn expression in bladder tissues.

    • Main Results:

    • MSA mice displayed inefficient and unstable bladder function, characterized by increased voiding contraction amplitude, frequent nonvoiding contractions, and elevated postvoid residual volume.
    • Bladder walls showed early detrusor and age-related urothelium hypertrophy.
    • Neuropathological findings included loss of parasympathetic neurons, PMC degeneration, and hαSyn expression in peripheral nerves of the bladder.

    Conclusions:

    • The PLP-hαSyn transgenic mouse model effectively recapitulates major urological symptoms observed in human MSA.
    • These urological deficits are associated with α-synuclein-related central and peripheral neuropathology.
    • This model serves as a valuable preclinical tool for elucidating the pathomechanisms of MSA-related urological failure.