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Aging and Alzheimer disease are associated with an accumulation of neuronal DNA double-strand breaks (DSBs). To learn more, researchers conducted a series of mouse experiments.
Exploring a novel environment for 2 hours or increasing neuronal activity through sensory or optogenetic stimulation increased markers of DSBs — but only in areas involved in learning, memory, and stimulus processing (e.g., dentate gyrus and visual cortex). DSBs were repaired after 24 hours of rest. Mice that were transgenic for human amyloid precursor protein (hAPP), an animal model of Alzheimer disease, had more DSBs before exploration, more severe and prolonged DSBs afterward, and less restoration after resting. Knocking out the tau protein normalized DSBs in hAPP …