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THE IMPACT OF CHRONIC STRESS ON CIRCADIAN RHYTHMS AND OXIDATIVE DNA DAMAGE IN THE HIPPOCAMPUS OF MICE
Selina Joy Freiand 11 co-authors
ETH Zürich
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS02-07PM-161
Presentation
Date TBA
Board: PS02-07PM-161
Event Information
Poster Board
PS02-07PM-161
Poster
View posterAbstract
Oxidative DNA damage poses a particular threat to neurons, which rely on stable, long‑lived genomes to maintain their function in the absence of cell division. Chronic stress can exacerbate this vulnerability by altering glucocorticoid exposure, increasing metabolic load, and disrupting circadian rhythms which are all processes that can influence oxidative balance and DNA repair capacity. The hippocampus, a region central to learning, memory, and stress adaptation, sits at the intersection of these signals and therefore provides a key context to investigate how stress can shape neuronal genome stability in dependence of the circadian rhythm.
Here, we investigate the impact of chronic stress on stress-related behaviors, steroid hormone-cycling and the accompanying transcriptional changes with a special focus on DNA repair pathways. We apply a recently published nucleotide-resolution mapping of one of the main putative target DNA lesions and study their interaction with diurnal cycling and epigenetic gene regulation. Lastly, we explore a direct axis that links glucocorticoid signaling with said DNA lesions. Our findings are expected to shed light on a putative circadian dependence of hippocampal genome maintenance and its vulnerability to chronic stress.
Here, we investigate the impact of chronic stress on stress-related behaviors, steroid hormone-cycling and the accompanying transcriptional changes with a special focus on DNA repair pathways. We apply a recently published nucleotide-resolution mapping of one of the main putative target DNA lesions and study their interaction with diurnal cycling and epigenetic gene regulation. Lastly, we explore a direct axis that links glucocorticoid signaling with said DNA lesions. Our findings are expected to shed light on a putative circadian dependence of hippocampal genome maintenance and its vulnerability to chronic stress.
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