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Cognitive and neurologic deficits in the MRL/lpr mouse: a clinicopathologic study
D C Hess1, M Taormina, J Thompson
1Department of Neurology, VA Medical Center, Augusta, GA 30910.
The Journal of Rheumatology
|April 1, 1993
Summary
The MRL/lpr mouse model exhibits neurological and cognitive deficits, potentially due to early central nervous system mononuclear cell infiltration, not cerebral infarction. This study explores neurological complications linked to antiphospholipid antibodies.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Antiphospholipid antibodies (aPL) are linked to neurological conditions like stroke and dementia.
- The MRL/lpr mouse strain produces high levels of anticardiolipin antibodies (aCL).
Purpose of the Study:
- To investigate neurological deficits in MRL/lpr mice and their pathological basis.
- To assess the MRL/lpr mouse as a model for antiphospholipid antibody-associated neurological complications.
Main Methods:
- A clinicopathologic study comparing MRL/lpr mice with MRL/+ mice at different ages (8-10 weeks and 16-20 weeks).
- Measurement of anticardiolipin antibodies (aCL) and anti-DNA antibodies via ELISA.
- Assessment of cognitive and sensorimotor functions using a water maze and neurological examination.
- Pathological examination of brains and cardiac valves.
Main Results:
- MRL/lpr mice showed elevated aCL levels and developed cognitive and sensorimotor deficits by 16 weeks.
- Poorer performance in the water maze was observed in MRL/lpr mice as early as 8 weeks.
- Mononuclear infiltrates were present in the choroid plexus of MRL/lpr mice, but no cerebral infarction or cardiac valve pathology was found.
Conclusions:
- MRL/lpr mice develop neurological and cognitive deficits, possibly due to early central nervous system mononuclear cell infiltration.
- Elevated aCL levels in MRL/lpr mice did not correlate with cerebral infarction or mitral valve abnormalities in this study.