ArticleInternational journal of clinical and experimental pathology2014
Electron microscopic features of brain edema in rodent cerebral malaria in relation to glial fibrillary acidic protein expression.
Article in International journal of clinical and experimental pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Modelling amoebic brain infection caused by Balamuthia mandrillaris using a human cerebral organoid.PLoS neglected tropical diseases · 2024Article
- Effects of anti-tau immunotherapy on reactive microgliosis, cerebral endotheliopathy, and cognitive function in an experimental model of cerebral malaria.Journal of neurochemistry · 2023Article
- Transcellular blood-brain barrier disruption in malaria-induced reversible brain edema.Life science alliance · 2022Article
- Melatonin Prevents Brain Damage and Neurocognitive Impairment Induced byFrontiers in cellular and infection microbiology · 2020Article
- Elimination of intravascular thrombi prevents early mortality and reduces gliosis in hyper-inflammatory experimental cerebral malaria.Journal of neuroinflammation · 2018Article
- Tissue-specific immunopathology during malaria infection.Nature reviews. Immunology · 2018Review
- Perivascular Arrest of CD8+ T Cells Is a Signature of Experimental Cerebral Malaria.PLoS pathogens · 2015Article
- Mitochondrial and cytoskeletal alterations are involved in the pathogenesis of hydronephrosis in ICR/Mlac-hydro mice.International journal of clinical and experimental medicine · 2015Article
- Cerebral malaria: gamma-interferon redux.Frontiers in cellular and infection microbiology · 2014Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms leading to cerebral malaria (CM) are not completely understood. Brain edema has been suggested as having an important role in experimental CM. In this study, CBA/CaH mice were infected with Plasmodium berghei ANKA blood-stage and when typical symptoms of CM developed on day 7, brain tissues were processed for electron-microscopic and immunohistochemical studies. The study demonstrated ultrastructural hallmarks of cerebral edema by perivascular edema and astroglial dilatation confirming existing evidence of vasogenic and cytogenic edema. This correlates closely with the clinical features of CM. An adaptive response of astrocytic activity, represented by increasing glial fibrillary acidic protein (GFAP) expression in the perivascular area and increasing numbers of large astrocyte clusters were predominately found in the CM mice. The presence of multivesicular and lamellar bodies indicates the severity of cerebral damage in experimental CM. Congestion of the microvessels with occluded white blood cells (WBCs), parasitized red blood cells (PRBCs) and platelets is also a crucial covariate role for CM pathogenesis.
Indexed as
Identifiers
24966914PMC4069908W2175814443What OpenQuestion holds
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.