alpha-synuclein and Malaria--Falciparum

Cerebral malaria, a reversible encephalopathy affecting young children, is a medical emergency requiring urgent clinical assessment and treatment. We performed a whole-transcriptomic analysis of blood samples from Malian children with cerebral or uncomplicated malaria. We focused on transcripts from pathways for which dysfunction has been associated with neurodegenerative disorders. We found that SNCA, SIAH2, UBB, HSPA1A, TUBB2A, and PINK1 were upregulated (fold-increases, ≥2.6), whereas UBD and PSMC5 were downregulated (fold-decreases, ≤4.39) in children with cerebral malaria, compared with those with uncomplicated malaria. These findings provide the first evidence for pathogenic mechanisms common to human cerebral malaria and neurodegenerative disorders.

Topics: Adaptor Proteins, Signal Transducing; alpha-Synuclein; ATPases Associated with Diverse Cellular Activities; Child; Child, Preschool; Down-Regulation; Female; Gene Expression Profiling; HSP70 Heat-Shock Proteins; Humans; Leukocytes, Mononuclear; LIM Domain Proteins; Malaria, Cerebral; Malaria, Falciparum; Male; Neurodegenerative Diseases; Nuclear Proteins; Plasmodium falciparum; Prospective Studies; Proteasome Endopeptidase Complex; Protein Kinases; Reproducibility of Results; Transcription Factors; Tubulin; Ubiquitin; Ubiquitin-Protein Ligases; Ubiquitins; Up-Regulation