Journal of photochemistry and photobiology. B, BiologyMay 5, 2026

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

Circadian Biology Weekly Brief ↗PubMed ↗DOI ↗

Updated Jun 27, 2026

Abstract

Essence

Artificial light at night impaired mouse memory alongside Bmal1-related hippocampal oxidative damage and neurogenesis disruption.

Evidence

Preclinical mouse study exposed C57BL/6 J mice to 28 days of 5-lx artificial light at night and used hippocampal AAV modulation of Bmal1 to test its role.

Caveat

The findings come from a mouse model with experimental light exposure and hippocampal gene manipulation, so they do not establish human cognitive effects.

Simplified

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.