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Complement C5-deficient mice are protected from seizures in experimental cerebral malaria
Susan C Buckingham1, Theresa N Ramos, Scott R Barnum
1Department of Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama, U.S.A.
Epilepsia
|November 12, 2014
Summary
The membrane attack complex (MAC) causes seizures. Inhibiting MAC formation in cerebral malaria models significantly reduced seizure activity, suggesting a therapeutic target.
Area of Science:
- Neuroscience
- Immunology
- Infectious Diseases
Background:
- The membrane attack complex (MAC) is known to induce seizures when directly applied to the brain.
- Experimental cerebral malaria (ECM) is associated with neurological complications, including seizures.
Purpose of the Study:
- To investigate the role of the MAC in seizures occurring during experimental cerebral malaria (ECM).
- To determine if inhibiting the terminal complement pathway affects seizure frequency in ECM.
Main Methods:
- Long-term video-electroencephalography (EEG) was used to monitor seizure activity.
- Comparison of seizure frequency between C5-deficient mice (lacking MAC formation) and wild-type mice infected with Plasmodium berghei ANKA.
Main Results:
- C5-deficient mice exhibited significantly reduced spike and seizure frequency compared to wild-type mice during ECM.
- This indicates a correlation between MAC formation and seizure activity in ECM.
Conclusions:
- The MAC plays a role in mediating seizures associated with malaria.
- Inhibiting the terminal complement pathway may be a viable strategy to reduce seizures and associated neurocognitive deficits in ECM.
