Early postinjury exercise reverses memory deficits and retards the progression of closed‐head injury in mice
Open accessAbstract
Key points: Exercise benefits the brain in many ways, e.g. promoting neuron repair and inhibiting neuroinflammation. However, current clinical practices often advise patients suffering head injury to rest during the post‐traumatic period. This study used a mouse model to investigate whether and how exercise retarded the brain structural and functional losses induced by a head impact. An early moderate‐exercise protocol (starting 2 days postimpact and lasting for 7 or 14 days) reversed the impact‐induced rapid loss of recognition memory and prevented most of the delayed neuronal loss and neuroinflammation. However, the same exercise protocol started 9 days postimpact was unable to restore deficits in the recognition memory, even though it still retarded the late‐phase neuroinflammation. These beneficial effects of exercise were probably mediated by the timely recovery of neurotrophic factors (brain‐derived neurotrophic factor and mitogen‐activated protein kinase phosphatase‐1) in the injured brain. Abstract Closed‐head injury (CHI) usually involves both physical damage of neurons and neuroinflammation. Although exercise promotes neuronal repair and suppresses neuroinflammation, CHI patients currently often remain resting during the post‐traumatic period. This study aimed to investigate whether and how postinjury exercise benefited the brain structure and function in mice after CHI. Closed‐head injury immediately caused an elevated neurological severity score, with rapid loss of object recognition memory, followed by progressive location‐dependent brain damage (neuronal loss and activation of microglia in the cortex and hippocampus). An early exercise protocol at moderate intensity (starting 2 days postimpact and lasting for 7 or 14 days) effectively restored the object recognition memory and prevented the progressive neuronal loss and activation of microglia. However, if the exercise started 9 days postimpact, it was unable to recover recognition memory deficits. In parallel, early exercise intervention drastically promoted neurite regeneration, while late exercise intervention was much less effective. We also tested the possible involvement of brain‐derived neurotrophic factor (BDNF) and mitogen‐activated protein kinase phosphatase‐1 (MKP‐1) in the exercise‐induced beneficial effects. Exercise gradually restored the impact‐abolished hippocampal expression of BDNF and MPK‐1, while oral administration of triptolide (a synthesis inhibitor of MKP‐1 and an antagonist of nuclear factor‐κB) before each bout of exercise blocked the restorative effects of exercise on MKP‐1 and recognition memory, as well as the exercise‐induced retardation of neuronal loss. Although triptolide treatment alone inhibited activation of microglia and maintained neuronal numbers, it did not recover the injury‐hampered recognition memory. Overall, moderate exercise shortly after CHI reversed the deficits in recognition memory and prevented the progression of brain injury.
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Early post-injury exercise reverses memory deficits and inhibits the progression of neurodegeneration following TBI.
“early post-injury exercise has been shown to reverse memory deficits and inhibit the progression of neurodegeneration following TBI [27].”
From The neuropathology of sport (2014) · cites this paper as [27]
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- Authors
- Chen, M., Huang, T., Kuo, Y., Yu, L., Chen, H., & Jen, C. J.
- Affiliations
- Institute of Basic Medical Sciences of the Chinese Academy of Medical Sciences (CN)
- ORCID
- Venue
- The Journal of Physiology
- Publisher
- Wiley
- Published
- 2013-01-11
- Volume
- 591
- Issue
- 4
- Pages
- 985-1000
- ISSN
- 0022-3751 (ISSN-L)
- 1469-7793
- PMC
- PMC3591710
- OpenAlex
- W1528048182
- Cited by
- 37
- References
- 51
- Citations by year
- 2025: 3 · 2024: 5 · 2023: 2 · 2022: 3 · 2021: 2 · 2020: 3 · 2019: 2 · 2018: 3 · 2017: 2 · 2016: 1 · 2015: 5 · 2014: 3 · 2013: 3
- FWCI
- 2.63
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Science Council
- Topics
- Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- closed head injury, memory impairment, object recognition memory, neuroinflammation, microglial activation, neuronal loss, brain-derived neurotrophic factor, MKP-1, triptolide, hippocampus, neurite regeneration, concussion rehabilitation, neuroprotection, NF-κB signaling
- MeSH terms
- Animals, Cerebral Cortex, Male, Memory Disorders, Mice, Inbred ICR, Neurons, Physical Conditioning, Animal, Head Injuries, Closed, Microglia, Brain-Derived Neurotrophic Factor, Recognition, Psychology, Mice, Dual Specificity Phosphatase 1, CA1 Region, Hippocampal
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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