Related Experiment Video
Updated: Jun 16, 2026
13:45
Evaluation of Extracellular Vesicle Function During Malaria Infection
Published on: February 14, 2018
Microvesiculation and cell interactions at the brain-endothelial interface in cerebral malaria pathogenesis.
Valéry Combes1, Fatima El-Assaad, Dorothée Faille
1Department of Pathology, Vascular Immunology Unit, Sydney Medical School, The University of Sydney, Australia.
Progress in Neurobiology
|February 2, 2010
Summary
Cerebral malaria (CM) pathogenesis involves neurovascular damage, particularly endothelial alteration. Targeting membrane microparticles (MP) shows promise in preventing neurological complications and mortality in CM.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Cerebral malaria (CM) remains a significant global health issue with poorly understood pathogenic mechanisms.
- Existing research highlights the importance of anti-malarial immunity and neurovascular aspects in CM.
Purpose of the Study:
- To elucidate the neurovascular aspects of cerebral malaria pathogenesis.
- To investigate the role of endothelial activation and alteration in CM.
- To explore the potential of targeting membrane microparticles (MP) as a therapeutic strategy.
Main Methods:
- Review of anti-malarial immunity and neurovascular aspects of CM.
- Analysis of "mediator-induced" and "host cell-induced" mechanisms of endothelial alteration.
- Evaluation of membrane microparticle (MP) pathogenic role in African patients and a mouse model.
- Intervention studies involving gene knockout and pharmacological inhibition of MP production.
Main Results:
- Endothelial activation and alteration are central to CM pathogenesis.
- Both "mediator-induced" (cytokines, chemokines) and "host cell-induced" (glial cells) mechanisms contribute to endothelial damage.
- Membrane microparticles (MP) play a pathogenic role in CM.
- Inhibition of MP production prevents neurological syndrome and reduces mortality in CM models.
Conclusions:
- Endothelial alteration is a key pathogenic mechanism in cerebral malaria.
- Membrane microparticles (MP) represent a potential therapeutic target for preventing CM-associated neurological complications and mortality.
- Further research into MP-targeted interventions could lead to novel treatments for cerebral malaria.
More Related Videos
09:04In Vivo Tracking of Edema Development and Microvascular Pathology in a Model of Experimental Cerebral Malaria Using Magnetic Resonance Imaging
Published on: June 8, 2017
12:48Isolation and Analysis of Brain-sequestered Leukocytes from Plasmodium berghei ANKA-infected Mice
Published on: January 2, 2013
Related Concept Videos
01:29Malaria
Malaria pathogenesis in humans reflects a delicate interplay between parasite biology and host response. Clinical illness reflects a host’s immune response to the parasite’s asexual replication cycle, which is often asymptomatic in individuals with partial immunity. From the parasite's perspective, transmission between mosquito and human with minimal host pathology is evolutionarily advantageous. Among the six Plasmodium species infecting humans, P. falciparum and P. vivax dominate in global...
01:22Cerebral Edema ll: Pathophysiology
Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
01:26Bacterial Meningitis II: Pathophysiology
Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
01:26Encephalitis ll: Pathophysiology
Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
01:18Viral Meningitis
Viral meningitis is the most common form of meningitis and is often referred to as aseptic meningitis to indicate the absence of bacterial involvement. It is generally milder than bacterial meningitis, with symptoms including fever, headache, stiff neck, drowsiness, nausea, photophobia, and vomiting. Rarely, more severe manifestations or death may occur. Common causative agents include enteroviruses, particularly coxsackie A and B viruses and echoviruses, all members of the Enterovirus genus...
01:29Hemorrhagic Stroke ll: Pathophysiology
A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...