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ePoster
NEIL3: FROM DNA REPAIR TO EPIGENETIC CONTROL OF MEMORY
Marion Silvana Fernandez Berrocaland 4 co-authors
NTNU
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS01-07AM-186
Presentation
Date TBA
Board: PS01-07AM-186
Event Information
Poster Board
PS01-07AM-186
Poster
View posterAbstract
Dynamic DNA methylation is essential for neural plasticity and memory, yet the link between genome integrity and epigenetic regulation remains poorly understood. NEIL enzymes, traditionally recognized for oxidative base excision repair (BER), have emerged as regulators of transcription and chromatin dynamics. Our recent work positions NEIL3 as a key modulator of hippocampal function beyond DNA repair, influencing neuronal maturation, adult neurogenesis, and excitatory/inhibitory balance.
Using Neil3 knockout models, we demonstrate that loss of NEIL3 alters hippocampal transcriptomes, disrupts oscillatory activity, and impairs cognitive processes such as contextual fear memory and pattern separation. Mechanistically, NEIL3 deficiency leads to hypermethylation of the Gabra2 promoter, reduced GABA receptor expression, and network-level dysfunction. While direct evidence for NEIL3-driven demethylation remains limited, our findings suggest NEIL3 may facilitate TDG-mediated DNA demethylation, linking genome maintenance to epigenetic control. Transcriptomic analyses reveal NEIL3-dependent pathways enriched for synaptic signaling and WNT-mediated neurogenesis.
Collectively, these studies establish NEIL3 as a bridge between DNA repair and neuroepigenetic regulation, providing a framework for understanding methylation dynamics in neurodevelopmental and neurodegenerative disorders.
Using Neil3 knockout models, we demonstrate that loss of NEIL3 alters hippocampal transcriptomes, disrupts oscillatory activity, and impairs cognitive processes such as contextual fear memory and pattern separation. Mechanistically, NEIL3 deficiency leads to hypermethylation of the Gabra2 promoter, reduced GABA receptor expression, and network-level dysfunction. While direct evidence for NEIL3-driven demethylation remains limited, our findings suggest NEIL3 may facilitate TDG-mediated DNA demethylation, linking genome maintenance to epigenetic control. Transcriptomic analyses reveal NEIL3-dependent pathways enriched for synaptic signaling and WNT-mediated neurogenesis.
Collectively, these studies establish NEIL3 as a bridge between DNA repair and neuroepigenetic regulation, providing a framework for understanding methylation dynamics in neurodevelopmental and neurodegenerative disorders.
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