Brain aging is associated with lower production of circadian clock proteins, which synchronize biological processes to light and dark cycles. In Alzheimer’s and other neurodegenerative diseases, circadian dysfunction is commonly observed.
In this study, a research team led by David Holtzman, M.D., of Washington University School of Medicine in St. Louis and Garret FitzGerald, M.D., of University of Pennsylvania’s Perelman School of Medicine, deleted (in mouse models) several genes that affect production of the clock proteins. This resulted in neurodegeneration including synaptic terminal degradation, impaired functional connectivity in the cortex, oxidative damage to neurons, and promotion of neuron death.
The researchers concluded that the genes expressing clock proteins are in fact important to brain homeostasis and recommend further study of circadian clock gene regulation, as it is possibly related to the progression of AD. This study identifies a potential therapeutic target: by bolstering expression of clock genes, we may be able to produce neuroprotective effects.
Read the full paper here: http://www.jci.org/articles/31868