TY - JOUR T1 - Little Exercise, Big Effects: Reversing Aging and Infection-Induced Memory Deficits, and Underlying Processes JF - The Journal of Neuroscience JO - J. Neurosci. SP - 11578 LP - 11586 DO - 10.1523/JNEUROSCI.2266-11.2011 VL - 31 IS - 32 AU - Ruth M. Barrientos AU - Matthew G. Frank AU - Nicole Y. Crysdale AU - Timothy R. Chapman AU - Jared T. Ahrendsen AU - Heidi E.W. Day AU - Serge Campeau AU - Linda R. Watkins AU - Susan L. Patterson AU - Steven F. Maier Y1 - 2011/08/10 UR - http://www.jneurosci.org/content/31/32/11578.abstract N2 - We have previously found that healthy aged rats are more likely to suffer profound memory impairments following a severe bacterial infection than are younger adult rats. Such a peripheral challenge is capable of producing a neuroinflammatory response, and in the aged brain this response is exaggerated and prolonged. Normal aging primes, or sensitizes, microglia, and this appears to be the source of this amplified inflammatory response. Among the outcomes of this exaggerated neuroinflammatory response are impairments in synaptic plasticity and reductions of brain-derived neurotrophic factor (BDNF), both of which have been associated with cognitive impairments. Since it has been shown that physical exercise increases BDNF mRNA in the hippocampus, the present study examined voluntary exercise in 24-month-old F344×BN rats as a neuroprotective therapeutic in our bacterial infection model. Although aged rats ran only an average of 0.7 km per week, this small amount of exercise was sufficient to completely reverse infection-induced impairments in hippocampus-dependent long-term memory compared with sedentary animals. Strikingly, exercise prevented the infection-induced exaggerated neuroinflammatory response and the blunted BDNF mRNA induction seen in the hippocampus of sedentary rats. Moreover, voluntary exercise abrogated age-related microglial sensitization, suggesting a possible mechanism for exercise-induced neuroprotection in aging. ER -