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Isolation and Analysis of Brain-sequestered Leukocytes from Plasmodium berghei ANKA-infected Mice
Published on: January 2, 2013
Cognitive dysfunction in mice infected with Plasmodium berghei strain ANKA
Mahalia S Desruisseaux1, Maria Gulinello, David N Smith
1Department of Pathology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
The Journal of Infectious Diseases
|April 19, 2008
Summary
Cerebral malaria impairs working memory in mice, showing cognitive deficits linked to brain inflammation and microglial changes. This model aids research into treatments for malaria-related neurological issues.
Area of Science:
- Neuroscience
- Infectious Diseases
- Immunology
Background:
- Cerebral malaria (CM) causes significant human morbidity with lasting cognitive problems.
- Understanding CM's neurological impact is crucial for developing effective treatments.
- Existing models require refinement to accurately assess cognitive sequelae.
Purpose of the Study:
- To establish a rodent model of cerebral malaria to study cognitive function.
- To investigate the relationship between CM, brain pathology, and cognitive impairment.
- To provide a platform for testing therapeutic interventions.
Main Methods:
- C57BL/6 mice were infected with Plasmodium berghei strain ANKA to induce cerebral malaria.
- Working memory was assessed using an object-recognition test 7 days post-infection.
- Brain pathology, including hemorrhage, inflammation, and microglial activity, was examined.
Main Results:
- Infected mice exhibited significant visual working memory deficits.
- Cognitive impairment correlated with cerebral hemorrhage and inflammation.
- Increased microglial activity and morphological changes were observed in infected brains, correlating with cognitive defects.
Conclusions:
- This murine model of cerebral malaria accurately reflects cognitive deficits seen in humans.
- The model demonstrates a link between cerebral inflammation, microglial changes, and cognitive dysfunction.
- This model is valuable for studying adjunctive therapies to mitigate adverse neurological outcomes in cerebral malaria.
