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Brain-Derived Neurotrophic Factor in Neonatal Seizures
Brennan J Sullivan1, Shilpa D Kadam2
1Neuroscience Laboratory, Hugo Moser Research Institute at Kennedy Krieger, Baltimore, Maryland.
Pediatric Neurology
|March 27, 2021
Summary
Brain-derived neurotrophic factor (BDNF) signaling is crucial for brain development. Excessive BDNF-tyrosine receptor kinase B (TrkB) activity may cause neonatal seizures, suggesting a new treatment target.
Area of Science:
- Neuroscience
- Developmental Biology
- Neurology
Background:
- Brain-derived neurotrophic factor (BDNF) is vital for neuronal development, survival, and plasticity.
- BDNF and its receptor, tyrosine receptor kinase B (TrkB), are critical for synapse formation and maturation.
- Research has primarily focused on decreased BDNF in neurological disorders, overlooking heightened activity.
Purpose of the Study:
- To review the role of BDNF-TrkB signaling in the immature brain.
- To examine the contribution of excessive BDNF-TrkB activity to refractory neonatal seizures.
- To explore targeting BDNF-TrkB signaling as a potential antiseizure therapy.
Main Methods:
- Literature review of preclinical and clinical studies.
- Critical analysis of existing research on BDNF-TrkB signaling pathways.
- Synthesis of findings related to neonatal seizures and BDNF-TrkB activity.
Main Results:
- Decreased BDNF is linked to synaptic deficits in neurological disorders.
- Excessive BDNF-TrkB signaling in the developing brain may induce hyperexcitability.
- This hyperexcitability is implicated in the pathophysiology of refractory neonatal seizures.
Conclusions:
- Heightened BDNF-TrkB signaling presents a potential mechanism for neonatal seizures.
- Targeting the BDNF-TrkB pathway offers a novel therapeutic avenue for refractory neonatal seizures.
- Further research is warranted to validate BDNF-TrkB as an antiseizure strategy.

