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Olfactory Assays for Mouse Models of Neurodegenerative Disease
Published on: August 25, 2014
Intact olfaction in a mouse model of multiple system atrophy
Florian Krismer1, Gregor K Wenning, Yuntao Li
1Division of Neurobiology, Department of Neurology, Innsbruck Medical University, Innsbruck, Austria.
Plos One
|May 22, 2013
Summary
Olfaction remains intact in a mouse model of multiple system atrophy (MSA) despite alpha-synuclein buildup in the olfactory bulb. This finding supports the human disorder
Area of Science:
- Neuroscience
- Olfactory Research
- Neurodegenerative Diseases
Background:
- Olfaction is typically preserved in human multiple system atrophy (MSA) patients, unlike Parkinson's disease patients who often experience hyposmia.
- Existing Parkinson's disease mouse models show olfactory deficits, but data for MSA models were previously unavailable.
Purpose of the Study:
- To investigate olfactory function and neuropathology in a transgenic mouse model of multiple system atrophy (MSA) with oligodendroglial alpha-synuclein overexpression.
- To compare olfactory behavior and olfactory bulb changes between transgenic MSA mice and wild-type controls.
Main Methods:
- A transgenic mouse model overexpressing alpha-synuclein in oligodendroglia was used.
- Olfactory preference testing was conducted in a pilot study.
- Long-term studies characterized age-related changes in the olfactory bulb.
Main Results:
- No significant differences in olfactory preference were observed between transgenic MSA mice and wild-type controls.
- Tyrosine hydroxylase-positive cell counts in the olfactory bulb remained unaffected.
- Despite age-related increases in alpha-synuclein within the olfactory bulb, progressive degeneration was not detected.
Conclusions:
- The transgenic MSA mouse model exhibits preserved olfaction, consistent with the human condition.
- This suggests a primary oligodendrogliopathy in MSA, with potentially variable neuronal involvement.
- Alpha-synucleinopathy in the olfactory bulb does not necessarily lead to olfactory deficits in this MSA model.
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