Long-term voluntary exercise inhibited AGE/RAGE and microglial activation and reduced the loss of dendritic spines in the hippocampi of APP/PS1 transgenic mice

Wang, Yiying; Zhou, Yuning; Jiang, Lin; Wang, Shun; Zhu, Lin; Zhang, Shanshan; Yang, Hao; He, Qi; Liu, Li; Xie, Yuhan; Liang, Xin; Tang, Jing; Chao, Feng‐lei; Tang, Yong

doi:10.1016/j.expneurol.2023.114371

Cited by 13 publications

(7 citation statements)

References 124 publications

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“…De Senna et al [35] and Chupel et al [36] demonstrated that exercise improves the level of inflammation in brain by safeguarding the structural integrity of the blood-brain barrier, which eventually leads to reduction of TNF-α and IL-6 expression. Our results are in line with clinical and animal studies [37,38] that have identified elevated levels of pro-inflammatory factors as a significant predictor of a wide range of neurodegeneration disorders and observed that exercise has anti-inflammatory effects.…”

Section: A B C D Esupporting

confidence: 92%

“…In this regard, it has been reported that synapse-related proteins depended on inflammatory response and the increase of cytokines such as TNF-α and IL-6 inhibits the expression of synapsin-1 and -2 in normal biological aging [ 44 ]. On the other hand, many studies indicated that long-term exercise might protect hippocampal by enhancing synaptic connections and either promotes synaptic formation and/or maintain synapses that would have otherwise alteration after brain damage [ 38 , 45 ]. Eventually, reduced inflammation and increased plasticity within hippocampus are thought to be crucial for cognitive function [ 46 , 47 ].…”

Section: Discussionmentioning

confidence: 99%

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Exercise alleviates cisplatin-induced toxicity in the hippocampus of mice by inhibiting neuroinflammation and improving synaptic plasticity

Park,

Ko,

Han

2024

Korean J Physiol Pharmacol

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Chemotherapy-induced cognitive impairment is recognized as the most typical symptom in patients with cancer that occurs during and following the chemotherapy treatment. Recently many studies focused on pharmaceutical strategies to control the chemotherapy side effects, however it is far from satisfactory. There may be a need for more effective treatment options. The aim of this study was to investigate the protective effect of exercise on cisplatin-induced neurotoxicity. Eight-week-old C57BL6 mice were separated into three group: normal control (CON, n = 8); cisplatin injection control (Cis-CON, n = 8); cisplatin with aerobic exercise (Cis-EXE, n = 8). Cisplatin was administered intraperitoneally at a dose of 3.5 mg/kg/day. The Cis-EXE group exercise by treadmill running (14–16 m/min for 45 min daily, 3 times/week) for 12 weeks. Compared to the CON group, the cisplatin injection groups showed significant decrease in body weight and food intake, indicating successful induction of cisplatin toxicity. The Cis-CON group showed significantly increased levels of pro-inflammatory cytokines including IL-6, IL-1β, and TNF-α in the hippocampus, while the Cis-EXE group was significantly decreased in the expression of IL-6, IL-1β, and TNF-α. In addition, compared to the CON group, the levels of synapse-related proteins including synapsin-1 and -2 were significantly reduced in the Cis-CON group, and there was a significant difference between the Cis-CON and Cis-EXE groups. Antioxidant and apoptosis factors were significantly improved in the Cis-EXE group compared with the Cis-CON group. This study suggest that exercise could be meaningful approach to prevent or improve cisplatin-induced cognitive impairment.

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Section: A B C D Esupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Exercise alleviates cisplatin-induced toxicity in the hippocampus of mice by inhibiting neuroinflammation and improving synaptic plasticity

Park,

Ko,

Han

2024

Korean J Physiol Pharmacol

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“…5xFAD is a new type of AD mouse model developed on the basis of APP/PS1 and has received widespread attention. In recent animal studies on AD, APP/PS1 mice was widely used as the AD model due to that they have the characteristics of AD well at the cellular and molecular levels [18][19][20]. We believe that APP/PS1 mice can meet our study.…”

Section: A Animal Preparationmentioning

confidence: 75%

“…With the accumulation of gene effects, typical features similar to AD can appear in pathology and learning cognitive abilities, effectively simulating the characteristics of AD. Many scholars have studied the treatment and pathogenesis of AD based on this model mouse, which has high application value [18][19][20]. However, it remains unclear how long-term low-intensity TUS modulates neural activity in the hippocampal brain region, which is closely related to learning and memory, of the APP/PS1 AD mouse model.…”

Section: Introductionmentioning

confidence: 99%

Modulatory Effect of Low-Intensity Transcranial Ultrasound Stimulation on Behaviour and Neural Oscillation in Mouse Models of Alzheimer’s Disease

Yang,

Yan,

et al. 2024

IEEE Trans. Neural Syst. Rehabil. Eng.

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Transcranial ultrasound stimulation (TUS) is a noninvasive brain neuromodulation technique. The application of TUS for Alzheimer's disease (AD) therapy has not been widely studied. In this study, a long-term course (28 days) of TUS was used to stimulate the hippocampus of APP/PS1 mice. We examined the modulatory effect of TUS on behavior and neural oscillation in AD mice. We found that TUS can (1) improve the learning and memory abilities of AD mice; (2) reduce the phase-amplitude coupling of delta-epsilon, delta-gamma and theta-gamma frequency bands of local field potential, and increase the relative power of epsilon frequency bands in AD mice; (3) reduce the spike firing rate of interneurons and inhibit the phase-locked angle deflection between the theta frequency bands and the spikes of the two types of neurons that develops with the progression of the disease in AD mice. In summary, we demonstrate that TUS could effectively improve cognitive behavior and modulate neural oscillation with AD.

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“…In terms of specific microglial parameters, conflicting evidence exists regarding the impact of exercise on microglial numbers in AD mice. Some studies suggest that exercise leads to a decrease in microglial numbers ( Ke et al, 2011 ; Leem et al, 2011 ; Rodríguez et al, 2015 ; Wang Y. et al, 2023 ; Yang et al, 2023 ), while others indicate an increase ( Elahi et al, 2016 ; Xu et al, 2016 ; Hashiguchi et al, 2020 ; Zhang S. et al, 2022 ; Campos et al, 2023 ), and some findings show no significant change in microglial density in AD mice ( Xu et al, 2018 ; Zhang J. et al, 2018 ; Ziegler-Waldkirch et al, 2018 ; Oroszi et al, 2023 ). In terms of microglial phenotype, exercise can regulate CD68+ ( Ziegler-Waldkirch et al, 2018 ; Zhang S. et al, 2022 ; Oroszi et al, 2023 ; Wang Y. et al, 2023 ), CD86+ ( Lu et al, 2017 ; Zhang et al, 2019 ; Feng et al, 2023 ; Yang et al, 2023 ), triggering receptor expressed on myeloid cells 2 (TREM2) ( Zhang L. et al, 2022 ) and inflammatory molecules ( Xu et al, 2016 , 2018 ; Nakanishi et al, 2021 ; Han et al, 2023 ) in AD rodent models.…”

Section: Physical Exercise Regulates Microglia In Neurodegenerative M...mentioning

confidence: 99%

Physical exercise regulates microglia in health and disease

Strohm,

Majewska

2024

Front. Neurosci.

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There is a well-established link between physical activity and brain health. As such, the effectiveness of physical exercise as a therapeutic strategy has been explored in a variety of neurological contexts. To determine the extent to which physical exercise could be most beneficial under different circumstances, studies are needed to uncover the underlying mechanisms behind the benefits of physical activity. Interest has grown in understanding how physical activity can regulate microglia, the resident immune cells of the central nervous system. Microglia are key mediators of neuroinflammatory processes and play a role in maintaining brain homeostasis in healthy and pathological settings. Here, we explore the evidence suggesting that physical activity has the potential to regulate microglia activity in various animal models. We emphasize key areas where future research could contribute to uncovering the therapeutic benefits of engaging in physical exercise.

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Long-term voluntary exercise inhibited AGE/RAGE and microglial activation and reduced the loss of dendritic spines in the hippocampi of APP/PS1 transgenic mice

Cited by 13 publications

References 124 publications

Exercise alleviates cisplatin-induced toxicity in the hippocampus of mice by inhibiting neuroinflammation and improving synaptic plasticity

Exercise alleviates cisplatin-induced toxicity in the hippocampus of mice by inhibiting neuroinflammation and improving synaptic plasticity

Modulatory Effect of Low-Intensity Transcranial Ultrasound Stimulation on Behaviour and Neural Oscillation in Mouse Models of Alzheimer’s Disease

Physical exercise regulates microglia in health and disease

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