Early postinjury exercise reverses memory deficits and retards the progression of closed‐head injury in mice

Chen, Meifeng; Huang, Tai Yin; Kuo, Yu Min; Yu, Lung; Chen, Hsiun Ing; Jen, Chauying J.

doi:10.1113/jphysiol.2012.241125

Cited by 32 publications

(24 citation statements)

References 51 publications

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“…Additionally, both diet and exercise has been proven to be an effective remediation technique following TBI (Griesbach et al, 2009; Wu et al, 2011; Ying et al, 2012; Tyagi et al, 2013). Increased exercise in rodents within 2 days after injury improved cognitive deficits associated with object recognition memory (Chen et al, 2012) while an exercise regimen 3 months after injury improved working memory (Piao et al, 2013). Similarly, environmental enrichment has also been shown to improve both recovery and cognition in male and female rats (Matter et al, 2011; Cheng et al, 2012; Monaco et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Robust training attenuates TBI-induced deficits in reference and working memory on the radial 8-arm maze

Sebastian¹,

Diallo²,

Ling³

et al. 2013

Front. Behav. Neurosci.

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Globally, it is estimated that nearly 10 million people sustain severe brain injuries leading to hospitalization and/or death every year. Amongst survivors, traumatic brain injury (TBI) results in a wide variety of physical, emotional and cognitive deficits. The most common cognitive deficit associated with TBI is memory loss, involving impairments in spatial reference and working memory. However, the majority of research thus far has characterized the deficits associated with TBI on either reference or working memory systems separately, without investigating how they interact within a single task. Thus, we examined the effects of TBI on short-term working and long-term reference memory using the radial 8-arm maze (RAM) with a sequence of four baited and four unbaited arms. Subjects were given 10 daily trials for 6 days followed by a memory retrieval test 2 weeks after training. Multiple training trials not only provide robust training, but also test the subjects' ability to frequently update short-term memory while learning the reference rules of the task. Our results show that TBI significantly impaired short-term working memory function on previously acquired spatial information but has little effect on long-term reference memory. Additionally, TBI significantly increased working memory errors during acquisition and reference memory errors during retention testing 2 weeks later. With a longer recovery period after TBI, the robust RAM training mitigated the reference memory deficit in retention but not the short-term working memory deficit during acquisition. These results identify the resiliency and vulnerabilities of short-term working and long-term reference memory to TBI in the context of robust training. The data highlight the role of cognitive training and other behavioral remediation strategies implicated in attenuating deficits associated with TBI.

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Section: Discussionmentioning

confidence: 99%

Robust training attenuates TBI-induced deficits in reference and working memory on the radial 8-arm maze

Sebastian¹,

Diallo²,

Ling³

et al. 2013

Front. Behav. Neurosci.

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“…In this study, exercise seems to influence microglia through increased expression of CX3CL1, which confers on microglia the ability to up-regulate NPC proliferation. In other studies, exercise in animals was found to decrease age-related basal microglial proliferation (Kohman et al, 2012), and to lower microglial activation in models of hypoxia (Lin et al, 2012), high-fat diet (Yi et al, 2012), tau overexpression (Leem et al, 2011), and closed-head injury (Chen et al, 2012), further supporting the notion that exercise can play a role in deactivating and de-priming microglia. The molecular mechanisms underlying how exercise mediates these effects will be a fascinating area for future study, and may discover agents that can elicit exercise-induced effects without the need for actual exercise.…”

Section: Can Microglia Be Rejuvenated?mentioning

confidence: 92%

Microglial aging in the healthy CNS: phenotypes, drivers, and rejuvenation

Wong¹

2013

Front. Cell. Neurosci.

190

178

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Neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and age-related macular degeneration (AMD), share two characteristics in common: (1) a disease prevalence that increases markedly with advancing age, and (2) neuroinflammatory changes in which microglia, the primary resident immune cell of the CNS, feature prominently. These characteristics have led to the hypothesis that pathogenic mechanisms underlying age-related neurodegenerative disease involve aging changes in microglia. If correct, targeting features of microglial senescence may constitute a feasible therapeutic strategy. This review explores this hypothesis and its implications by considering the current knowledge on how microglia undergo change during aging and how the emergence of these aging phenotypes relate to significant alterations in microglial function. Evidence and theories on cellular mechanisms implicated in driving senescence in microglia are reviewed, as are “rejuvenative” measures and strategies that aim to reverse or ameliorate the aging microglial phenotype. Understanding and controlling microglial aging may represent an opportunity for elucidating disease mechanisms and for formulating novel therapies.

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“…Treadmill exercise also improves hippocampus-dependent spatial learning and memory as well as aversive memory [2, 3, 25, 97, 112, 174, 186, 187]. Furthermore, in rodent models, BDNF, insulin– like growth factor 1 (IGF-1), mitogen-activated protein kinase phosphatase-1 (MKP-1), and glial-derived neurotrophic factor (GDNP) are elevated by exercise [1, 53, 179] and early post-injury exercise has been shown to reverse memory deficits and inhibit the progression of neurodegeneration following TBI [27]. …”

Section: The Benefits Of Exercise and Sports Participationmentioning

confidence: 99%

The neuropathology of sport

et al. 2013

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The benefits of regular exercise, physical fitness and sports participation on cardiovascular and brain health are undeniable. Physical activity reduces the risk for cardiovascular disease, type 2 diabetes, hypertension, obesity, and stroke, and produces beneficial effects on cholesterol levels, antioxidant systems, inflammation, and vascular function. Exercise also enhances psychological health, reduces age-related loss of brain volume, improves cognition, reduces the risk of developing dementia, and impedes neurodegeneration. Nonetheless, the play of sports is associated with risks, including a risk for mild TBI (mTBI) and, rarely, catastrophic traumatic injury and death. There is also growing awareness that repetitive mTBIs, such as concussion and subconcussion, can occasionally produce persistent cognitive, behavioral, and psychiatric problems as well as lead to the development of a neurodegeneration, chronic traumatic encephalopathy (CTE). In this review, we summarize the beneficial aspects of sports participation on psychological, emotional, physical and cognitive health, and specifically analyze some of the less common adverse neuropathological outcomes, including concussion, second-impact syndrome, juvenile head trauma syndrome, catastrophic sudden death, and CTE. CTE is a latent neurodegeneration clinically associated with behavioral changes, executive dysfunction and cognitive impairments, and pathologically characterized by frontal and temporal lobe atrophy, neuronal and axonal loss, and abnormal deposits of paired helical filament (PHF)-tau and 43 kDa TAR deoxyribonucleic acid (DNA)-binding protein (TDP-43). CTE often occurs as a sole diagnosis, but may be associated with other neurodegenerative disorders, including motor neuron disease (CTE-MND). Although the incidence and prevalence of CTE are not known, CTE has been reported most frequently in American football players and boxers. Other sports associated with CTE include ice hockey, professional wrestling, soccer, rugby, and baseball.

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Early postinjury exercise reverses memory deficits and retards the progression of closed‐head injury in mice

Cited by 32 publications

References 51 publications

Robust training attenuates TBI-induced deficits in reference and working memory on the radial 8-arm maze

Robust training attenuates TBI-induced deficits in reference and working memory on the radial 8-arm maze

Microglial aging in the healthy CNS: phenotypes, drivers, and rejuvenation

The neuropathology of sport

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