UCLA

Due to the cyclical nature of selective pressures in our physical world, most organisms evolved endogenous circadian timing systems that generate circadian rhythms in behavior and physiology. External stimuli such as light can reset these rhythms allowing the synchronization of the body with the external environment. Symptoms of disrupted circadian systems are comorbid with both neurodegenerative and neurodevelopmental disease states. Deficits in the ability of light information to reach the circadian system may provide a mechanistic explanation for the deregulated circadian system. Our study investigated the presence of deficits in the light input pathway to the circadian system in Huntington’s Disease (HD) and Fragile X Syndrome (FXS) mouse models. We found that the ability of light information to reach the circadian system is not altered in these models and the observed circadian dysfunction may be due to an underlying pathology present in the central circadian circuit.