ReviewBrain pathology (Zurich, Switzerland)1997
Cerebral malaria.
Review in Brain pathology (Zurich, Switzerland), 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
50 citing papers in PubMed.
- DC8 and DC13 var genes associated with severe malaria bind avidly to diverse endothelial cells.PLoS pathogens · 2013Trial
- Malignant malaria: autopsy findings and morphological features.Malaria journal · 2026Article
- Expression of sphingosine-1-phosphate receptor 1 in the brain of fatal cerebral malaria.Scientific reports · 2026Article
- Transcellular blood-brain barrier disruption in malaria-induced reversible brain edema.Life science alliance · 2022Article
- Pathophysiology and neurologic sequelae of cerebral malaria.Malaria journal · 2020Review
- The malaria toxin hemozoin induces apoptosis in human neurons and astrocytes: Potential role in the pathogenesis of cerebral malaria.Brain research · 2019Article
- Proteomic profiling of the plasma of Gambian children with cerebral malaria.Malaria journal · 2018Article
- Elimination of intravascular thrombi prevents early mortality and reduces gliosis in hyper-inflammatory experimental cerebral malaria.Journal of neuroinflammation · 2018Article
- Neurovascular sequestration in paediatriceLife · 2018Article
- Adjunctive therapy for severe malaria: a review and critical appraisal.Malaria journal · 2018Review
- Signaling Strategies of Malaria Parasite for Its Survival, Proliferation, and Infection during Erythrocytic Stage.Frontiers in immunology · 2017Review
- A semi-synthetic glycosaminoglycan analogue inhibits and reverses Plasmodium falciparum cytoadherence.PloS one · 2017Article
- Deterioration of red blood cell mechanical properties is reduced in anaerobic storage.Blood transfusion = Trasfusione del sangue · 2016Article
- Cerebral malaria in children: using the retina to study the brain.Brain : a journal of neurology · 2014Review
- Intracerebral bleed, right haemiparesis and seizures: an atypical presentation of vivax malaria.BMJ case reports · 2014Article
- Disseminated intravascular coagulation in malaria: A case report.Nigerian medical journal : journal of the Nigeria Medical Association · 2014Article
- Experimental Models of Microvascular Immunopathology: The Example of Cerebral Malaria.Journal of neuroinfectious diseases · 2014Article
- Neuregulin-1 attenuates mortality associated with experimental cerebral malaria.Journal of neuroinflammation · 2014Article
- In vitro study of parasite elimination and endothelial protection by curcumin: adjunctive therapy for cerebral malaria.EXCLI journal · 2014Article
- The Case for the Use of PPARγ Agonists as an Adjunctive Therapy for Cerebral Malaria.PPAR research · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malaria infection of the Central Nervous System (CNS) can cause a severe neurological syndrome termed Cerebral Malaria (CM). The central neuropathological feature of CM is the preferential sequestration of parasitised red blood cells (PRBC) in the cerebral microvasculature. The level of sequestration is related to the incidence of cerebral symptoms in severe malaria. Other neuropathological features of CM include petechial hemorrhages in the brain parenchyma, ring hemorrhages and Dürck's granuloma's. Immunohisto-chemical and electron microscopy studies have shown widespread cerebral endothelial cell activation and morphological changes occur in CM, as well as focal endothelial cell damage and necrosis. The immune cell response to intravascular sequestration appears to be limited, although activation of pigment-phagocytosing monocytes is a late feature. The mechanisms by which PRBC cause coma in malaria remain unclear. In vitro parasitised erythrocytes bind to endothelial cells by specific, receptor mediated interactions with host adhesion molecules such as ICAM-1, whose expression on cerebral endothelial cells is increased during CM as part of a systemic endothelial activation. Induction of local neuro-active mediators such as nitric oxide and systemic cytokines like TNF alpha may be responsible for the rapidly reversible symptoms of the coma of CM. The recent cloning of the parasite ligand PfEMP-1, thought to mediate binding to host sequestration receptors, promises further insight into the relationship between patterns of sequestration and the incidence and pathogenesis of coma in cerebral malaria.
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Registered trials
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.