Although transcriptional responsiveness varies over the lifetime, many brain genes still seem to be responsive to exercise in old animals and in animal models for neurodegenerative diseases. Using the senescence-accelerated SAMP8 mouse a non-transgenic model for studying aspects of progressive cognitive decline and Alzheimerâs disease (AD) we have recently shown that exercise training during adulthood (6 months of voluntary training on a running wheel, 3 alternate days per week) prevented or delayed processes associated with aging. Unveiling the exercise-responsive mechanisms of chromatin regulation and their pathophysiological implications may lead to the development of new preventive and/or therapeutic interventions for age-related disorders, including neurodegenerative conditions.
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Last date updated on September, 2014