ArticleInternational journal of clinical and experimental pathology2011
Quantitation of brain edema and localisation of aquaporin 4 expression in relation to susceptibility to experimental cerebral malaria.
Article in International journal of clinical and experimental pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 36 citations in OpenAlex.
- Mechanisms of parasite-mediated disruption of brain vessels.FEBS letters · 2026Review
- β-Dystroglycan Downregulation and Astrocytic Alterations: A Possible Role in Blood-Brain Barrier Disruption During Experimental Cerebral Malaria.Molecular neurobiology · 2025Article
- Non-cerebral malaria: does such a thing exist?Memorias do Instituto Oswaldo Cruz · 2025Review
- Characterization of experimental cerebral malaria by volumetric MRI A comparative study across the sexes.PloS one · 2025Article
- Pathogenetic mechanisms and treatment targets in cerebral malaria.Nature reviews. Neurology · 2023Review
- Early therapeutic effects of an Angiopoietin-1 mimetic peptide in middle-aged rats with vascular dementia.Frontiers in aging neuroscience · 2023Article
- Cytoskeletal Alteration Is an Early Cellular Response in Pulmonary Epithelium Infected with Aspergillus fumigatus Rather than Scedosporium apiospermum.Microbial ecology · 2022Article
- The Glymphatic System (En)during Inflammation.International journal of molecular sciences · 2021Review
- Global and Regional Changes in Perivascular Space in Idiopathic and Familial Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2021Article
- The Potential Roles of Glial Cells in the Neuropathogenesis of Cerebral Malaria.Frontiers in cellular and infection microbiology · 2021Review
- Diabetic rats are more susceptible to cognitive decline in a model of microemboli-mediated vascular contributions to cognitive impairment and dementia.Brain research · 2020Article
- Experimental Scedosporiosis Induces Cerebral Oedema Associated with Abscess regarding Aquaporin-4 and Nrf-2 Depletions.BioMed research international · 2019Article
- Tissue-specific immunopathology during malaria infection.Nature reviews. Immunology · 2018Review
- Cerebral Malaria in Mouse and Man.Frontiers in immunology · 2018Review
- White matter damage and glymphatic dysfunction in a model of vascular dementia in rats with no prior vascular pathologies.Neurobiology of aging · 2017Article
- A potential role for interleukin-33 and γ-epithelium sodium channel in the pathogenesis of human malaria associated lung injury.Malaria journal · 2015Article
- The critical role of lipopolysaccharide in the upregulation of aquaporin 4 in glial cells treated with Shiga toxin.Journal of biomedical science · 2015Article
- Experimental cerebral malaria pathogenesis--hemodynamics at the blood brain barrier.PLoS pathogens · 2014Article
- A comprehensive analysis of aquaporin and secretory related gene expression in neonate and adult cholangiocytes.Gene expression patterns : GEP · 2014Article
- Production, fate and pathogenicity of plasma microparticles in murine cerebral malaria.PLoS pathogens · 2014Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenic mechanisms underlying the occurrence of cerebral malaria (CM) are still incompletely understood but, clearly, cerebral complications may result from concomitant microvessel obstruction and inflammation. The extent to which brain edema contributes to pathology has not been investigated. Using the model of P. berghei ANKA infection, we compared brain microvessel morphology of CM-susceptible and CM-resistant mice. By quantitative planimetry, we provide evidence that CM is characterized by enlarged perivascular spaces (PVS). We show a dramatic aquaporin 4 (AQP4) upregulation, selectively at the level of astrocytic foot processes, in both CM and non-CM disease, but significantly more pronounced in mice with malarial-induced neurological syndrome. This suggests that a threshold of AQP4 expression is needed to lead to neurovascular pathology, a view that is supported by significantly higher levels in mice with clinically overt CM. Numbers of intravascular leukocytes significantly correlated with both PVS enlargement and AQP4 overexpression. Thus, brain edema could be a contributing factor in CM pathogenesis and AQP4, specifically in its astrocytic location, a key molecule in this mechanism. Since experimental CM is associated with substantial brain edema, it models paediatric CM better than the adult syndrome and it is tempting to evaluate AQP4 in the former context. If AQP4 changes are confirmed in human CM, it may represent a novel target for therapeutic intervention.
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Identifiers
21904632PMC3160608W1873191394What OpenQuestion holds
Registered trials
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