Running exercise delays neurodegeneration in amygdala and hippocampus of Alzheimer’s disease (APP/PS1) transgenic mice

Lin, Tzu Wei; Shih, Ying-Hsia; Chen, Shean Jen; Lien, Chi-Hsiang; Chang, Chia Yuan; Huang, Tai Yin; Chen, Shun Hua; Jen, Chauying J.; Kuo, Yu Min

doi:10.1016/j.nlm.2014.12.005

Cited by 135 publications

(96 citation statements)

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“…Moore et al (2015) reported that three months of treadmill training, by three month old Tg2576 mice, upregulated proteins associated with proteolytic degradation of A␤ (neprilysin, matrix metallopeptidase 9 and insulin degrading enzyme), A␤ efflux across the blood-brain barrier (Low density lipoprotein receptor-related protein-1 (LRP-1)), and cellular uptake (heat shock protein 70) in a dose-dependent manner. Lin et al (2015) also observed an upregulation of LRP-1 in the amygdala and hippocampus of APP SWE /PS-1 E9 mice trained on a treadmill for three and a half months. While other mechanisms may yet be elucidated, exercise-mediated effects on mechanisms of amyloid degradation and clearance provide a plausible means by which this peripheral factor can alter AD neuropathology in transgenic models.…”

Section: Ad Pathologymentioning

confidence: 67%

“…Firstly, mice generally travel greater distances when given access to a running wheel. Typically they run four-five km per day (Clark et al, 2009(Clark et al, , 2008Garrett et al, 2012;Patten et al, 2013;van Praag et al, 1999a) compared to mice on treadmills which typically run 280-700 m per day (Koo et al, 2013;Lin et al, 2015;Yuede et al, 2009;Zhao et al, 2015). Obviously, mice running on treadmills are unable to reach the distances that mice exercising voluntarily on a running wheel can achieve.…”

Section: Discussionmentioning

confidence: 99%

“…From the few studies to date that have examined exercise-induced effects on hippocampal neurogenesis in AD mouse models, it is clear that neurogenic deficits can be effectively modulated by this intervention. Moreover, particularly in the APP SWE /PS-1 E9 mice, enhanced neurogenesis has been observed alongside cognitive improvements (Lin et al, 2015;Tapia-Rojas et al, 2016;Zhao et al, 2015), highlighting the key link between the two processes in the AD model of cognitive dysfunction. Assessments of hippocampal neurogenesis in addition to cognitive function in transgenic mouse models of AD given access to exercise would add greatly to our knowledge of the therapeutic or neuroprotective potential of physical activity in AD.…”

Section: Hippocampal Neurogenesismentioning

confidence: 95%

“…Spatial learning and memory (Adlard et al, 2005;Liu et al, 2011), contextual memory (Lin et al, 2015) and recognition memory (Yuede et al, 2009) are all improved following exercise training. However, Xu et al (2013), having failed to observe an exercise-induced amelioration of AD pathology, also found that six weeks of wheel running did not improve the performance of APP SWE /PS-1 E9 mice in the MWM.…”

Section: Cognitive Functionmentioning

confidence: 95%

“…However, to date all studies that have examined neurogenesis report pro-neurogenic effects. Synaptic plasticity (Zhao et al, 2015), dendritic arborisation (Lin et al, 2015), cell proliferation and neuronal differentiation (Tapia-Rojas et al, 2016) are all increased in APP SWE /PS-1 E9 mice that have undergone exercise training. Yuede et al (2009) report increased hippocampal volume in five month old Tg2576 mice housed with a running wheel or exercised on a treadmill for 16 weeks.…”

Section: Hippocampal Neurogenesismentioning

confidence: 99%

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Exercise as a pro-cognitive, pro-neurogenic and anti-inflammatory intervention in transgenic mouse models of Alzheimer’s disease

Ryan

Kelly

2016

Ageing Research Reviews

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a b s t r a c tIt is now well established, at least in animal models, that exercise elicits potent pro-cognitive and proneurogenic effects. Alzheimer's disease (AD) is one of the leading causes of dementia and represents one of the greatest burdens on healthcare systems worldwide, with no effective treatment for the disease to date. Exercise presents a promising non-pharmacological option to potentially delay the onset of or slow down the progression of AD. Exercise interventions in mouse models of AD have been explored and have been found to reduce amyloid pathology and improve cognitive function. More recent studies have expanded the research question by investigating potential pro-neurogenic and anti-inflammatory effects of exercise. In this review we summarise studies that have examined exercise-mediated effects on AD pathology, cognitive function, hippocampal neurogenesis and neuroinflammation in transgenic mouse models of AD. Furthermore, we attempt to identify the optimum exercise conditions required to elicit the greatest benefits, taking into account age and pathology of the model, as well as type and duration of exercise.© 2016 Elsevier B.V. All rights reserved. Please cite this article in press as: Ryan, S.M., Kelly, Á.M., Exercise as a pro-cognitive, pro-neurogenic and anti-inflammatory intervention in transgenic mouse models of Alzheimer's disease. Ageing Res. Rev. (2016), http://dx

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Section: Ad Pathologymentioning

confidence: 67%

Section: Discussionmentioning

confidence: 99%

Section: Hippocampal Neurogenesismentioning

confidence: 95%

Section: Cognitive Functionmentioning

confidence: 95%

Section: Hippocampal Neurogenesismentioning

confidence: 99%

See 3 more Smart Citations

Exercise as a pro-cognitive, pro-neurogenic and anti-inflammatory intervention in transgenic mouse models of Alzheimer’s disease

Ryan

Kelly

2016

Ageing Research Reviews

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Levels of Physical Activity at Age 10 Years and Brain Morphology Changes From Ages 10 to 14 Years

Estévez-López,

Dall’Aglio,

Rodriguez-Ayllon

et al. 2023

JAMA Netw Open

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ImportancePhysical activity may promote healthy brain development in children, but previous research was predominantly cross-sectional and included small samples, providing limited knowledge.ObjectiveTo investigate the longitudinal associations of physical activity with brain morphology changes.Design, Setting, and ParticipantsA 4-year longitudinal population-based cohort study in Rotterdam, the Netherlands, embedded in Generation R, a cohort from fetal life onward. From the women enrolled during pregnancy, children who had repeated measures of brain structure at ages 10 (range 8 to 12) years and 14 (range 13 to 15) years were included. Data were collected from March 2013 to November 2015 (baseline) and from October 2016 to January 2020 (follow-up). Data were analyzed from April to December 2022.ExposureAt age 10 years, both the child and their primary caregiver reported the child’s levels of physical activity with regard to sport participation, outdoor play, and total physical activity. Primary analyses were based on an average multi-informant report.Main outcomes and measuresBrain morphology was quantified by magnetic resonance imaging. Hypothesized regions of interest were the bilateral amygdala and hippocampal volumes. Global brain measures were studied to test the specificity of the hypothesis.ResultsData were available for 1088 children (566 girls [52%]; 693 [64%] Dutch). Their mean (SD) age at baseline was 10.1 (0.6) years. For amygdala volume change, positive associations with multi-informant reports of total physical activity (β = 2.6; 95% CI, 0.3-4.9) were found. Total physical activity was associated with hippocampal volume increases only when reported by the child (β = 3.1; 95% CI, 0.4-5.8). No robust associations with global brain measures were found.Conclusions and relevanceIn this cohort study of 1088 children, more physical activity at 10 years was consistently associated with an increase in amygdala volume in children aged 10 to 14 years. Physical activity and increases in hippocampal volume were found using child reports of physical activity only. These findings suggest physical activity in late childhood was prospectively associated with volumetric changes in specific subcortical structures, but not to global brain development, from late childhood to early adolescence. These findings may inform the design of future public health interventions to best facilitate neurodevelopment with physical activity.

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Activity‐Dependent Induction of Younger Biological Phenotypes

Lissek

2022

Advanced Biology

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In several mammalian species, including humans, complex stimulation patterns such as cognitive and physical exercise lead to improvements in organ function, organism health and performance, as well as possibly longer lifespans. A framework is introduced here in which activity‐dependent transcriptional programs, induced by these environmental stimuli, move somatic cells such as neurons and muscle cells toward a state that resembles younger cells to allow remodeling and adaptation of the organism. This cellular adaptation program targets several process classes that are heavily implicated in aging, such as mitochondrial metabolism, cell–cell communication, and epigenetic information processing, and leads to functional improvements in these areas. The activity‐dependent gene program (ADGP) can be seen as a natural, endogenous cellular reprogramming mechanism that provides deep insight into the principles of inducible improvements in cell and organism function and can guide the development of therapeutic approaches for longevity. Here, these ADGPs are analyzed, exemplary critical molecular nexus points such as cAMP response element‐binding protein, myocyte enhancer factor 2, serum response factor, and c‐Fos are identified, and it is explored how one may leverage them to prevent, attenuate, and reverse human aging‐related decline of body function.

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Running exercise delays neurodegeneration in amygdala and hippocampus of Alzheimer’s disease (APP/PS1) transgenic mice

Cited by 135 publications

References 64 publications

Exercise as a pro-cognitive, pro-neurogenic and anti-inflammatory intervention in transgenic mouse models of Alzheimer’s disease

Exercise as a pro-cognitive, pro-neurogenic and anti-inflammatory intervention in transgenic mouse models of Alzheimer’s disease

Levels of Physical Activity at Age 10 Years and Brain Morphology Changes From Ages 10 to 14 Years

Activity‐Dependent Induction of Younger Biological Phenotypes

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