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Updated: Jul 5, 2026

Assessment of Sensorimotor Function in Mouse Models of Parkinson's Disease
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MsrA knockout mouse exhibits abnormal behavior and brain dopamine levels.

Derek B Oien1, Greg L Osterhaus, Shaheen A Latif

  • 1Department of Pharmacology and Toxicology, School of Pharmacy, University of Kansas, Lawrence, KS 66045, USA.

Free Radical Biology & Medicine
|May 10, 2008
PubMed
Summary

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Methionine sulfoxide reductase A knockout mice show impaired learning and motor activity. Their dopamine levels and signaling pathways are altered, suggesting relevance to age-related neurological diseases linked to oxidative stress.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Oxidative Stress Research

Background:

  • Oxidative stress leads to methionine oxidation, potentially causing protein malfunction.
  • Methionine sulfoxide reductase A (MsrA) deficiency is linked to brain pathologies and abnormal gait.
  • Oxidized methionine residues are increasingly found in neurodegenerative conditions.

Purpose of the Study:

  • To investigate the impact of MsrA deficiency on complex task learning, locomotor activity, and gait.
  • To explore the age-dependent changes in brain dopamine levels and release in MsrA knockout mice.
  • To determine the relationship between MsrA deficiency, dopamine regulation, and age-related neurological dysfunction.

Main Methods:

  • Behavioral analysis of MsrA knockout (MsrA(-/-)) mice, including complex task learning and locomotor activity assessment.

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  • Age-dependent measurement of dopamine levels and release in the brains of MsrA(-/-) mice.
  • Analysis of tyrosine hydroxylase activating protein expression in relation to dopamine levels.

    • Main Results:

    • MsrA(-/-) mice exhibited compromised complex task learning, reduced locomotor activity, and age-exacerbated gait alterations.
    • Dopamine levels were elevated in young MsrA(-/-) mice but decreased in older mice compared to wild-type.
    • Increased dopamine release and altered tyrosine hydroxylase activating protein expression were observed, correlating with age-dependent dopamine changes.

    Conclusions:

    • MsrA deficiency impairs cognitive and motor functions, potentially due to dysregulated dopamine pathways.
    • Age-dependent alterations in dopamine regulation in MsrA(-/-) mice may contribute to neurological deficits.
    • These findings highlight the role of MsrA in mitigating oxidative stress-induced neurological damage and suggest relevance to age-related neurodegenerative diseases.