Exercise Reverses Amyloid β-Peptide–Mediated Cognitive Deficits in Alzheimer’s Disease Mice Expressing Mutant Presenilin-2

Hwang, Dong-Joo; Choi, Donghoon; Kwon, Ki-Chun; Kim, Eon-Ho; Kim, Tae‐Kyung; Koo, Jung-Hoon; Cho, Joon-Yong

doi:10.1249/mss.0000000000002834

Cited by 5 publications

(7 citation statements)

References 56 publications

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“…The transcriptomic analysis revealed that in AD mice the cell cycle regulatory gene, Cdc28 protein kinase regulatory subunit 2 (Cks2), was decreased while some cell cycle and apoptotic cell death-related factors, including cyclin D1, proliferating cell nuclear antigen, and cleaved caspase-3, were increased in the hippocampus of Tg-PS2m. The treadmill exercise reversed the altered expressions ( Hwang et al, 2022 ).…”

Section: Resultsmentioning

confidence: 97%

“…Exercise can boost memory and dampen brain inflammation ( De Miguel et al, 2021 ). The pathologic features and behavioral symptoms of AD caused by the accumulation of amyloid β-peptide in the hippocampus can be reversed by regular exercise ( Hwang et al, 2022 ). Additionally, exercise could promote the motoneuron survival in ALS animals, protect against 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicity in the model mice of PD ( Gerecke et al, 2010 ), and ameliorate striatal deficits in HD model mice ( Pang et al, 2006 ).…”

Section: Introductionmentioning

confidence: 99%

“…Exercise intervention has many advantages. First, exercise is a non-invasive intervention, which will not cause additional pain and wounds to patients ( Hwang et al, 2022 ). Compared with drugs and surgery, exercise intervention is more easily accepted by most patients.…”

Section: Introductionmentioning

confidence: 99%

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Multi-omics studies reveal ameliorating effects of physical exercise on neurodegenerative diseases

Guo

Wang²,

Chao³

et al. 2022

Front. Aging Neurosci.

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IntroductionNeurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and Huntington’s disease, are heavy burdens to global health and economic development worldwide. Mounting evidence suggests that exercise, a type of non-invasive intervention, has a positive impact on the life quality of elderly with neurodegenerative diseases. X-omics are powerful tools for mapping global biochemical changes in disease and treatment.MethodThree major databases were searched related to current studies in exercise intervention on neurodegenerative diseases using omics tools, including metabolomics, metagenomics, genomics, transcriptomics, and proteomics.ResultWe summarized the omics features and potential mechanisms associated with exercise and neurodegenerative diseases in the current studies. Three main mechanisms by which exercise affects neurodegenerative diseases were summed up, including adult neurogenesis, brain-derived neurotrophic factor (BDNF) signaling, and short-chain fatty acids (SCFAs) metabolism.ConclusionOverall, there is compelling evidence that exercise intervention is a feasible way of preventing the onset and alleviating the severity of neurodegenerative diseases. These studies highlight the importance of exercise as a complementary approach to the treatment and intervention of neurodegenerative diseases in addition to traditional treatments. More mechanisms on exercise interventions for neurodegenerative diseases, the specification of exercise prescriptions, and differentiated exercise programs should be explored so that they can actually be applied to the clinic.

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Section: Resultsmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

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Multi-omics studies reveal ameliorating effects of physical exercise on neurodegenerative diseases

Guo

Wang²,

Chao³

et al. 2022

Front. Aging Neurosci.

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“…Recently, Hwang et al evaluated the effect of regular moderate-intensity exercise on improving cognitive function in a mouse model of AD [ 83 ]. Specifically, four groups of mice were included: a control group; a group expressing human wild type presenilin-2 (PS-2), a protein that when mutated determines the onset of AD; a group expressing mutated human PS-2; and a group expressing mutated human PS-2 but subjected to treadmill exercise 50 min a day, 5 days a week, for a total of 6 weeks.…”

Section: Physical Exercise As a Non-pharmacological Strategy To Preve...mentioning

confidence: 99%

“…Interestingly, the group of transgenic animals subjected to exercise showed a greater aptitude for exploring new objects than the untrained transgenic mice. Furthermore, transcriptomic analysis showed an increased expression of factors associated with apoptotic death in the untrained mouse model of AD, suggesting that regular exercise may reverse cellular abnormalities caused by Aβ deposition [ 83 ].…”

Section: Physical Exercise As a Non-pharmacological Strategy To Preve...mentioning

confidence: 99%

Physical Exercise and Health: A Focus on Its Protective Role in Neurodegenerative Diseases

Bonanni

Cariati

Tarantino

et al. 2022

JFMK

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Scientific evidence has demonstrated the power of physical exercise in the prevention and treatment of numerous chronic and/or age-related diseases, such as musculoskeletal, metabolic, and cardiovascular disorders. In addition, regular exercise is known to play a key role in the context of neurodegenerative diseases, as it helps to reduce the risk of their onset and counteracts their progression. However, the underlying molecular mechanisms have not yet been fully elucidated. In this regard, neurotrophins, such as brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), glia cell line-derived neurotrophic factor (GDNF), neurotrophin-3 (NT-3), and neurotrophin-4 (NT-4), have been suggested as key mediators of brain health benefits, as they are involved in neurogenesis, neuronal survival, and synaptic plasticity. The production of these neurotrophic factors, known to be increased by physical exercise, is downregulated in neurodegenerative disorders, suggesting their fundamental importance in maintaining brain health. However, the mechanism by which physical exercise promotes the production of neurotrophins remains to be understood, posing limits on their use for the development of potential therapeutic strategies for the treatment of neurodegenerative diseases. In this literature review, we analyzed the most recent evidence regarding the relationship between physical exercise, neurotrophins, and brain health, providing an overview of their involvement in the onset and progression of neurodegeneration.

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Muscle Psn gene combined with exercise contribute to healthy aging of skeletal muscle and lifespan by adaptively regulating Sirt1/PGC-1α and arm pathway

Gao,

Wen,

et al. 2024

PLoS ONE

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The Presenilin (Psn) gene is closely related to aging, but it is still unclear the role of Psn genes in skeletal muscle. Here, the Psn-UAS/Mhc-GAL4 system in Drosophila was used to regulate muscle Psn overexpression(MPO) and muscle Psn knockdown(MPK). Drosophila were subjected to endurance exercise from 4 weeks to 5 weeks old. The results showed that MPO and exercise significantly increased climbing speed, climbing endurance, lifespan, muscle SOD activity, Psn expression, Sirt1 expression, PGC-1α expression, and armadillo (arm) expression in aged Drosophila, and they significantly decreased muscle malondialdehyde levels. Interestingly, when the Psn gene is knockdown by 0.78 times, the PGC-1α expression and arm expression were also down-regulated, but the exercise capacity and lifespan were increased. Furthermore, exercise combined with MPO further improved the exercise capacity and lifespan. MPK combined with exercise further improves the exercise capacity and lifespan. Thus, current results confirmed that the muscle Psn gene was a vital gene that contributed to the healthy aging of skeletal muscle since whether it was overexpressed or knocked down, the aging progress of skeletal muscle structure and function was slowed down by regulating the activity homeostasis of Sirt1/PGC-1α pathway and Psn/arm pathway. Exercise enhanced the function of the Psn gene to delay skeletal muscle aging by up regulating the activity of the Sirt1/PGC-1α pathway and Psn/arm pathway.

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Exercise Reverses Amyloid β-Peptide–Mediated Cognitive Deficits in Alzheimer’s Disease Mice Expressing Mutant Presenilin-2

Cited by 5 publications

References 56 publications

Multi-omics studies reveal ameliorating effects of physical exercise on neurodegenerative diseases

Multi-omics studies reveal ameliorating effects of physical exercise on neurodegenerative diseases

Physical Exercise and Health: A Focus on Its Protective Role in Neurodegenerative Diseases

Muscle Psn gene combined with exercise contribute to healthy aging of skeletal muscle and lifespan by adaptively regulating Sirt1/PGC-1α and arm pathway

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