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Altered olfactory function in the MRL model of CNS lupus
Minesh Kapadia1, Mile Stanojcic, Aoife M Earls
1The Brain-Body Institute, St. Joseph's Healthcare, McMaster University, Hamilton, Ontario, Canada.
Behavioural Brain Research
|July 17, 2012
Summary
Systemic lupus erythematosus (SLE) can cause olfactory deficits in patients. Autoimmune MRL/lpr mice also show impaired odor-guided behaviors and altered neuronal precursor cell migration, suggesting a link between SLE and olfactory dysfunction.
Area of Science:
- Neuroimmunology
- Autoimmune Diseases
- Neuroscience
Background:
- Systemic lupus erythematosus (SLE) is a chronic autoimmune disease affecting multiple organs, including the central nervous system (CNS).
- CNS involvement in SLE can lead to brain atrophy and neuropsychiatric symptoms.
- Olfactory deficits have been anecdotally reported in SLE patients with CNS complications.
Purpose of the Study:
- To investigate olfactory dysfunction in MRL/lpr mice, a model for spontaneous lupus-like disease.
- To determine if autoimmune processes in SLE impact odor-guided behaviors and olfactory system neurogenesis.
Main Methods:
- Utilized a battery of odor-guided behavioral paradigms to assess olfactory function in lupus-prone MRL/lpr mice.
- Examined the distribution of Doublecortin-positive (DCX+) cells, a marker for neuronal precursor cells, in the rostral migratory stream (RMS).
Main Results:
- Lupus-prone male mice exhibited reduced exploration of unfamiliar conspecifics.
- Mice showed age-dependent deficits in discriminating low concentrations of odors.
- Olfactory changes correlated with altered DCX+ cell distribution in the RMS, indicating disrupted neurogenesis.
Conclusions:
- The findings support the hypothesis that SLE-like conditions affect periventricular brain regions, including the RMS.
- Disrupted migration of neuronal precursor cells may underlie olfactory deficits in autoimmune disease.
- Hyposmia and olfactory memory deficits could be early indicators of CNS damage in SLE.
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