Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 197, Issue 11, Pages 1621-1627Publisher
UNIV CHICAGO PRESS
DOI: 10.1086/587908
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Funding
- NHLBI NIH HHS [T32 HL-07675, T32 HL007675, T32 HL007675-20] Funding Source: Medline
- NIAID NIH HHS [P30 AI051519-06, P30 AI051519] Funding Source: Medline
- NIMHD NIH HHS [L32 MD002222] Funding Source: Medline
- NINDS NIH HHS [R01 NS041282, R01 NS041282-06] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
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Cerebral malaria complicated by cognitive sequelae is a major cause of morbidity in humans infected with Plasmodium falciparum. To model cognitive function after malaria, we created a rodent model of cerebral malaria by infecting C57BL/6 mice with Plasmodium berghei strain ANKA. After 7 days, an object-recognition test of working memory revealed a significant impairment in the visual memory of infected mice. This impairment was observed in the absence of confounding effects of infection. The cognitive dysfunction correlated with hemorrhage and inflammation. Furthermore, microglial activity and morphological changes detected throughout the brains of infected mice were absent from the brains of control mice, and this correlated with the measured cognitive defects. Similar testing methods in human studies could help identify subjects at risk for an adverse cognitive outcome. This murine model should facilitate the study of adjunctive methods to ameliorate adverse neurological outcomes in cerebral malaria.
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