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Little exercise, big effects: reversing aging and infection-induced memory deficits, and underlying processes.

ABSTRACT: 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.

SUBMITTER: Barrientos RM

PROVIDER: S-EPMC3171131 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:The present study examined mechanisms underlying memory deficits in Parkinson's disease (PD) and their associations with brain structural metrics. Nineteen PD patients and twenty-two matched controls underwent two memory experiments. In Experiment 1 (delayed memory task), subjects were asked to remember an array of colored rectangles with varying memory set sizes (Low-Load (2 items), Low-Load (relevant 2 items) with Distractor (irrelevant 3 items), and High-Load (5 items)). After a 7 s delay period, they reported whether the orientation of any relevant figures had changed (test period). In Experiment 2 (working memory task), memory arrays were presented in varying set sizes (2 to 6 items) without distractors, followed by a 2 s delay period and a subsequent test period. Brain MRI data were acquired to assess structural differences (volumes and cortical thickness) in areas related to attention, working memory storage capacity, and episodic memory. Multivariate analyses of covariance revealed that, compared with controls, PD patients had lower memory capacity scores in all memory load conditions for Experiment 1 (p < 0.021), whereas there were no group differences in any memory load conditions for Experiment 2 (p > 0.06). In addition, PD patients had lower cortical thickness in the left superior temporal gyrus (p = 0.02), a region related to the ventral attentional system. Moreover, regression analyses revealed that lower cortical thickness values in the left superior temporal gyrus significantly predicted lower memory scores of Low-Load and Low-Load with Distractor conditions in Experiment 1 (p < 0.044) and lower scores of memory load conditions of 4 and 5 items in Experiment 2 (p < 0.012). These findings suggest that memory deficits in PD may partly be due to impaired attentional filtering and memory consolidation processes that may be related to superior temporal neurodegeneration. Future studies are warranted to confirm the current findings to guide the development of effective treatments for memory deficits in PD.

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Little exercise, big effects: reversing aging and infection-induced memory deficits, and underlying processes.

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