Publications by authors named "J Fraering"

Article Synopsis
  • Cerebral malaria (CM) is a severe and often fatal complication of Plasmodium falciparum malaria, impacting 15-25% of affected children even with treatment available.
  • A study investigating the infected erythrocytes and plasma of 24 Beninese children revealed significant changes in protein levels linked to CM, including a decrease in proteins from the ubiquitin-proteasome pathway and an increase in transferrin receptor protein 1 (TFRC).
  • The findings suggest that CM parasites may primarily infect young red blood cells and alter their development, with the plasma proteome reflecting specific markers for severe malaria that could lead to new diagnostic and prognostic tools.
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Cerebral malaria (CM) is the severest form of Plasmodium falciparum infection. Children under 5 years old are those most vulnerable to CM, and they consequently have the highest risk of malaria-related death. Parasite-associated factors leading to CM are not yet fully elucidated.

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PfEMP1 is the major antigen involved in -infected erythrocyte sequestration in cerebrovascular endothelium. While some PfEMP1 domains have been associated with clinical phenotypes of malaria, formal associations between the expression of a specific domain and the adhesion properties of clinical isolates are limited. In this context, 73 cerebral malaria (CM) and 98 uncomplicated malaria (UM) Beninese children were recruited.

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Generation of amyloid-β peptides (Aβs) by proteolytic cleavage of the amyloid-β protein precursor (AβPP), especially increased production of Aβ42/Aβ43 over Aβ40, and their aggregation as oligomers and plaques, represent a characteristic feature of Alzheimer's disease (AD). In familial AD (FAD), altered Aβ production originates from specific mutations of AβPP or presenilins 1/2 (PS1/PS2), the catalytic subunits of γ-secretase. In sporadic AD, the origin of altered production of Aβs remains unknown.

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