ArticlePLoS pathogens2010
Cognitive dysfunction is sustained after rescue therapy in experimental cerebral malaria, and is reduced by additive antioxidant therapy.
Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 125 citations in OpenAlex.
- Beyond the mouse: organoids, spheroids, and organs-on-chips as the (inevitable) future of malaria research?Malaria journal · 2026Review
- Evaluation of clinically approved neuroprotective drugs as adjunct therapies in experimental cerebral malaria.Archives of microbiology · 2026Article
- Lycopene Mitigates Malaria-Induced Reactive Oxygen and Nitrogen Species and Oxidative Damage in Mice Brain and Lungs.Parasite immunology · 2025Article
- Polycyclitol Derivatives Restore Long- Term Memory Via cdk5/p25 Activation of Tau Signaling in Experimental Cerebral Malaria.Neurochemical research · 2025Article
- Self-assembling dendrimer nanodrug formulations for decreased hERG-related toxicity and enhanced therapeutic efficacy.Science advances · 2025Article
- Non-cerebral malaria: does such a thing exist?Memorias do Instituto Oswaldo Cruz · 2025Review
- Article
- Emerging drugs for the treatment of herpetic keratitis.Expert opinion on emerging drugs · 2024Review
- Synthesis and antimalarial activity of amide and ester conjugates of siderophores and ozonides.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2023Article
- Interplay Between the Immune and Nervous Cognitive Systems in Homeostasis and in Malaria.International journal of biological sciences · 2023Review
- Investigation of Plasma-Derived Lipidome Profiles in Experimental Cerebral Malaria in a Mouse Model Study.International journal of molecular sciences · 2022Article
- Co-administration of chloroquine and coenzyme QJournal of parasitic diseases : official organ of the Indian Society for Parasitology · 2022Article
- Oxidative Stress in Malaria: Potential Benefits of Antioxidant Therapy.International journal of molecular sciences · 2022Review
- NADPH Oxidase: a Possible Therapeutic Target for Cognitive Impairment in Experimental Cerebral Malaria.Molecular neurobiology · 2022Article
- Cerebral Malaria: Current Clinical and Immunological Aspects.Frontiers in immunology · 2022Review
- Dynamics and immunomodulation of cognitive deficits and behavioral changes in non-severe experimental malaria.Frontiers in immunology · 2022Article
- Current Understanding of Long-Term Cognitive Impairment After Sepsis.Frontiers in immunology · 2022Review
- Malaria Related Neurocognitive Deficits and Behavioral Alterations.Frontiers in cellular and infection microbiology · 2022Review
- Immune system challenge improves recognition memory and reverses malaria-induced cognitive impairment in mice.Scientific reports · 2021Article
- Oxidative Stress and Pathogenesis in Malaria.Frontiers in cellular and infection microbiology · 2021Review
8 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 5 institutions in 2 countries.
Funding
Abstract
Neurological impairments are frequently detected in children surviving cerebral malaria (CM), the most severe neurological complication of infection with Plasmodium falciparum. The pathophysiology and therapy of long lasting cognitive deficits in malaria patients after treatment of the parasitic disease is a critical area of investigation. In the present study we used several models of experimental malaria with differential features to investigate persistent cognitive damage after rescue treatment. Infection of C57BL/6 and Swiss (SW) mice with Plasmodium berghei ANKA (PbA) or a lethal strain of Plasmodium yoelii XL (PyXL), respectively, resulted in documented CM and sustained persistent cognitive damage detected by a battery of behavioral tests after cure of the acute parasitic disease with chloroquine therapy. Strikingly, cognitive impairment was still present 30 days after the initial infection. In contrast, BALB/c mice infected with PbA, C57BL6 infected with Plasmodium chabaudi chabaudi and SW infected with non lethal Plasmodium yoelii NXL (PyNXL) did not develop signs of CM, were cured of the acute parasitic infection by chloroquine, and showed no persistent cognitive impairment. Reactive oxygen species have been reported to mediate neurological injury in CM. Increased production of malondialdehyde (MDA) and conjugated dienes was detected in the brains of PbA-infected C57BL/6 mice with CM, indicating high oxidative stress. Treatment of PbA-infected C57BL/6 mice with additive antioxidants together with chloroquine at the first signs of CM prevented the development of persistent cognitive damage. These studies provide new insights into the natural history of cognitive dysfunction after rescue therapy for CM that may have clinical relevance, and may also be relevant to cerebral sequelae of sepsis and other disorders.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.