, Erik Musiek and colleagues at Washington University School of Medicine asked whether BMAL1 and the rest of the core clock contribute to the maintenance of healthy neurons. Using
-deficient mice, the authors found that as these mice aged activated astrocytes began to accumulate, a hallmark of active inflammation and damage.
-deficient mice also displayed localized degeneration of neuronal cells and a loss of functional connectivity, as measured by blood flow.
The researchers found that BMAL1 and the other activating core clock proteins regulate important redox proteins that prevent damage caused by oxidative stress. In an accompanying commentary, Colleen McClung from the University of Pittsburgh noted that the activating circadian core clock proteins could be explored as targets for future therapies for neurodegenerative diseases.