Nighttime artificial blue light exposure is significantly associated with adolescent depression, and mechanistically operates through a lactic acid-ALKBH5-m6A axis that disrupts neuronal plasticity in the lateral habenula.
Prolonged nighttime device use exceeding 4 hours was significantly associated with depressive symptoms in adolescents.
Blue light exposure during sleep (BLS) induced depression-like behaviors in rodents.
Blue light exposure during sleep elevated lactic acid levels in the lateral habenula (LHb) in rodents.
Upregulation of ALKBH5 in the lateral habenula modified N6-methyladenosine (m6A) levels and disrupted neuronal plasticity.
LHb-specific ALKBH5 knockdown reduced both behavioral and synaptic abnormalities in the rodent model.
Peripheral blood samples from adolescents with high nighttime artificial blue light exposure (NABLE) exhibited increased ALKBH5 expression.
Nighttime artificial blue light exposure (NABLE) was identified as a potential independent risk factor for depression in adolescents.
This research suggests that exposure to blue light from screens and nightlights during the nighttime hours is meaningfully linked to depression in teenagers. A case-control study found that adolescents who used devices for more than 4 hours at night, used high blue-light display settings, or slept with a nightlight on were significantly more likely to show signs of depression — and this connection held up even after accounting for differences in sleep habits and other personal factors. Machine learning tools analyzing the data independently confirmed that nighttime blue light exposure ranked among the strongest predictors of depressive symptoms. To understand how blue light might cause depression, the researchers investigated the biological chain of events in rodents. They found that blue light exposure during sleep raised levels of lactic acid in a brain region called the lateral habenula, which plays a known role in mood regulation. This lactic acid accumulation triggered increases in a protein called ALKBH5, which acts as an eraser of a type of chemical tag on RNA molecules (called m6A methylation). Disrupting these tags appears to impair the brain's ability to maintain healthy connections between neurons — a process called neuroplasticity — ultimately producing depression-like behavior. When researchers specifically blocked ALKBH5 activity in the lateral habenula, both the behavioral signs of depression and the abnormalities in brain cell connections were reduced. Importantly, teenagers with the highest levels of nighttime blue light exposure also showed elevated ALKBH5 in their blood, suggesting this same biological pathway may operate in humans. This research suggests that managing nighttime exposure to blue light — particularly from screens — could be a practical strategy for protecting adolescent mental health. The findings point to a specific molecular pathway (lactic acid → ALKBH5 → m6A modification → impaired neuroplasticity) that connects an everyday environmental exposure to the biology of depression, and highlight ALKBH5 as a potential biological marker and possible future therapeutic target for environmentally driven depression.
Li Y, Wang Y, Ma Y, Yang W, Yu G, Li H, et al.. (2026). Role of lactic acid-mediated ALKBH5 in depression induced by blue light exposure at night.. Ecotoxicology and environmental safety. https://doi.org/10.1016/j.ecoenv.2026.119928