Bmal1 regulates hippocampal oxidative damage in cognitive memory impairment induced by artificial light at night in mice

May 5, 2026Journal of photochemistry and photobiology. B, Biology

Bmal1 controls brain cell damage in memory problems caused by artificial light at night in mice

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Abstract

Exposure to 5-lux artificial light at night for 28 consecutive days induces cognitive impairment in mice.

Cognitive impairment was observed following prolonged exposure to artificial light at night.
ALAN exposure reduced the expression of Bmal1, a gene associated with circadian rhythms.
Increased levels of reactive oxygen species (ROS) and malondialdehyde were detected, indicating oxidative stress.
Disruption of time-of-day-dependent expression of NRF2, SOD1, and GPX1 was noted following ALAN exposure.
Reduced activity of antioxidant enzymes SOD and GPX was linked to oxidative damage in the hippocampus.
Modulating Bmal1 expression influenced levels of hippocampal apoptosis, affecting neurogenesis and memory.

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Artificial light at night (ALAN) has emerged as a significant public health concern, yet its effects on cognitive impairment remain poorly understood. This study investigated the impact of 28 consecutive days of 5-lx ALAN exposure on hippocampal function in C57BL/6 J mice. We evaluated locomotor behavior, neuronal morphology, neurogenesis, oxidative stress, and circadian rhythms, revealing that ALAN induces cognitive impairment. ALAN exposure reduced Bmal1 expression, increased reactive oxygen species (ROS) and malondialdehyde accumulation, and disrupted the time-of-day-dependent differences expression of NRF2, SOD1, and GPX1. These alterations suppressed SOD and GPX enzymatic activity, leading to hippocampal oxidative damage. To clarify BMAL1's role, we used adeno-associated virus (AAV) to modulate Bmal1 expression in the hippocampus. ALAN increased hippocampal apoptosis, which was exacerbated by Bmal1 knockdown and mitigated by its overexpression. These findings suggest that ALAN can contribute to memory impairment by disrupting hippocampal damage and impairing neurogenesis through its effect on Bmal1. This study identifies potential molecular targets for preventing and treating cognitive impairment and neurodegenerative disorders.

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Bmal1 regulates hippocampal oxidative damage in cognitive memory impairment induced by artificial light at night in mice

Abstract

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