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Activated microglia in acute encephalopathy with biphasic seizures and late reduced diffusion
Yuji Fujita1, Jun-Ichi Takanashi2, Haruka Takei1
1Department of Pediatrics, Teikyo University Chiba Medical Center, Ichihara, Japan.
Abstract:
Acute encephalopathy with biphasic seizures and late reduced diffusion (AESD) is the most common subtype of infectious pediatric encephalopathy in Japan. The exact pathogenesis of and the best therapeutic strategy for AESD are uncertain. We firstly performed a brain biopsy in a 2-year-old boy with AESD associated with RS viral infection, which revealed activated ameoboid microglia accumulation around degenerated neuron, and astrogliosis in the affected cortex. Glutamate released from activated microglia may play an important role in the pathogenesis of AESD, which is compatible with the previous report of magnetic resonance spectroscopy showing elevated glutamate.
Insights
Acute encephalopathy with biphasic seizures and late reduced diffusion (AESD) is a common pediatric brain condition. Brain biopsy revealed microglia activation and neuron damage, suggesting glutamate
Area of Science:
- Neurology
- Pediatrics
- Neuroscience
Background:
- Acute encephalopathy with biphasic seizures and late reduced diffusion (AESD) is the most frequent subtype of infectious pediatric encephalopathy in Japan.
- The precise pathogenesis and optimal therapeutic strategies for AESD remain unclear.
Observation:
- A brain biopsy was performed on a 2-year-old boy diagnosed with AESD and RS viral infection.
- The biopsy revealed activated amoeboid microglia surrounding degenerated neurons and astrogliosis in the affected cortical areas.
Findings:
- The accumulation of activated microglia suggests a significant inflammatory response in the affected brain tissue.
- The findings support the hypothesis that glutamate released from activated microglia may contribute to the pathogenesis of AESD.
Implications:
- This study provides crucial histopathological evidence for understanding AESD pathogenesis.
- Targeting microglial activation and glutamate pathways could be potential therapeutic strategies for AESD.
