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Little exercise, big effects: reversing aging and infection-induced memory deficits, and underlying processes
Ruth M Barrientos1, Matthew G Frank, Nicole Y Crysdale
1Department of Psychology and Neuroscience, University of Colorado at Boulder, Boulder, Colorado 80309, USA. ruth.barrientos@colorado.edu
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.
Insights
Even mild voluntary exercise in aged rats reversed memory loss caused by bacterial infection. This physical activity also prevented neuroinflammation and preserved brain-derived neurotrophic factor (BDNF) levels.
Area of Science:
- Neuroscience
- Immunology
- Gerontology
Background:
- Aging exacerbates neuroinflammation following peripheral infection, leading to memory deficits.
- Microglial sensitization in aged brains amplifies inflammatory responses.
- Reduced brain-derived neurotrophic factor (BDNF) and impaired synaptic plasticity are linked to cognitive decline.
Purpose of the Study:
- To investigate the neuroprotective effects of voluntary exercise in aged rats against infection-induced cognitive impairment.
- To determine if exercise can mitigate exaggerated neuroinflammation and BDNF reduction post-infection in aging.
Main Methods:
- 24-month-old F344×BN rats were subjected to a bacterial infection model.
- One group of rats engaged in voluntary exercise, while a control group remained sedentary.
- Hippocampus-dependent memory, neuroinflammatory markers, BDNF mRNA levels, and microglial sensitization were assessed.
Main Results:
- Voluntary exercise, even at low intensity (0.7 km/week), completely reversed infection-induced memory impairments in aged rats.
- Exercise prevented the exaggerated neuroinflammatory response and blunted BDNF mRNA induction observed in sedentary infected rats.
- Voluntary exercise abrogated age-related microglial sensitization, suggesting a key mechanism for neuroprotection.
Conclusions:
- Voluntary exercise is a potent neuroprotective strategy against infection-induced cognitive deficits in aging.
- Exercise mitigates neuroinflammation and preserves BDNF levels by reducing microglial sensitization.
- Physical activity may offer a therapeutic approach to combat age-related cognitive decline and infection vulnerability.
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