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Updated: Mar 26, 2026

Isolation and Analysis of Brain-sequestered Leukocytes from Plasmodium berghei ANKA-infected Mice
Published on: January 2, 2013
Increased synapsin I expression in cerebral malaria
Klairoong Thonsranoi1, Supattra Glaharn1, Chuchard Punsawad2
1Department of Tropical Pathology, Faculty of Tropical Medicine, Mahidol University Bangkok 10400, Thailand.
Cerebral malaria (CM) significantly increases synapsin I expression in cerebellar granule cells, correlating with parasite levels. This suggests CM may cause pre-synaptic excitation and altered neurotransmitter release, highlighting synapsin I as a potential therapeutic target.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Synapsin I is a key neuronal phosphoprotein regulating neurotransmitter release and synaptic formation.
- Neurological complications in severe malaria suggest neurotransmitter release abnormalities.
- Understanding synapsin I's role in cerebral malaria (CM) is crucial for addressing neurological deficits.
Purpose of the Study:
- To evaluate synapsin I expression in the brains of cerebral malaria patients.
- To compare synapsin I levels in CM, non-cerebral malaria (NCM), and control brain tissues.
- To investigate the correlation between parasitemia and synapsin I expression in CM.
Main Methods:
- Immunohistochemical analysis of synapsin I expression in post-mortem brain tissues.
- Semi-quantitative and qualitative assessment of synapsin I in CM (10 cases), NCM (4 cases), and control (5 cases) groups.
- Statistical analysis including Spearman correlation to assess relationships between parasitemia and synapsin I levels.
Main Results:
- Synapsin I expression was similar in the cerebral cortex and cerebellar molecular layer across all groups.
- A significant increase in synapsin I expression was observed in cerebellar granule cells and the glomerular synaptic complex in CM patients compared to NCM and controls (P < 0.05).
- Parasitemia positively correlated with synapsin I expression in granule cells and the glomerular synaptic complex in CM patients.
Conclusions:
- Cerebral malaria is associated with significantly elevated synapsin I expression in specific cerebellar regions.
- Increased synapsin I expression in CM suggests pre-synaptic excitation and enhanced neurotransmitter release.
- Targeting synapsin I may offer a therapeutic strategy for alleviating neurological symptoms in severe malaria.
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