Acute exercise does not modify brain activity and memory performance in APP/PS1 mice

Stein, Angélica Miki; Munive, Victor; Fernández, Adolfo; Núñez, Ángel; Torres‐Alemán, Ignacio

doi:10.1371/journal.pone.0178247

Cited by 20 publications

(11 citation statements)

References 51 publications

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“…Moreover, IGF-I administration can prevent loss of cognitive performance in humans [ 51 ]. According to these findings, our previous studies have also indicated that an IGF-I increase induced by exercise improves memory in young mice [ 52 ].…”

Section: Discussionsupporting

confidence: 56%

Response Facilitation Induced by Insulin-like Growth Factor-I in the Primary Somatosensory Cortex of Mice Was Reduced in Aging

García-Magro

Zegarra-Valdivia

Troyas-Martinez

et al. 2022

Cells

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Aging is accompanied by a decline in cognition that can be due to a lower IGF-I level. We studied response facilitation induced in primary somatosensory (S1) cortical neurons by repetitive stimulation of whiskers in young and old mice. Layer 2/3 and 5/6 neurons were extracellularly recorded in young (≤ 6 months of age) and old (≥ 20 month of age) anesthetized mice. IGF-I injection in S1 cortex (10 nM; 0.2 μL) increased whisker responses in young and old animals. A stimulation train at 8 Hz induced a long-lasting response facilitation in only layer 2/3 neurons of young animals. However, all cortical neurons from young and old animals showed long-lasting response facilitation when IGF-I was applied in the S1 cortex. The reduction in response facilitation in old animals can be due to a reduction in the IGF-I receptors as was indicated by the immunohistochemistry study. Furthermore, a reduction in the performance of a whisker discrimination task was observed in old animals. In conclusion, our findings indicate that there is a reduction in the synaptic plasticity of S1 neurons during aging that can be recovered by IGF-I. Therefore, it opens the possibility of use IGF-I as a therapeutic tool to ameliorate the effects of heathy aging.

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Section: Discussionsupporting

confidence: 56%

Response Facilitation Induced by Insulin-like Growth Factor-I in the Primary Somatosensory Cortex of Mice Was Reduced in Aging

García-Magro

Zegarra-Valdivia

Troyas-Martinez

et al. 2022

Cells

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“…Whether the exercise intervention is applied chronically or acutely also seems to be an important factor determining whether a benefit is derived in mice with AD. This was shown recently by Stein et al who showed an acute bout of exercise was beneficial in littermate WT controls, improving spatial memory, but had no effect in AD transgenic mice [ 106 ]. These findings support the findings in human studies which suggest A

pathology is not a reliable predictor of cognition in patients with AD, and that other factors such as neurogenesis may play larger roles in modulating cognitive decline.…”

Section: Exercise and Ad Protectionmentioning

confidence: 79%

The Protective Effect of Exercise in Neurodegenerative Diseases: The Potential Role of Extracellular Vesicles

Fuller

Whitham

Mathivanan

et al. 2020

Cells

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Physical activity has systemic effects on the body, affecting almost every organ. It is important not only for general health and wellbeing, but also in the prevention of diseases. The mechanisms behind the therapeutic effects of physical activity are not completely understood; however, studies indicate these benefits are not confined to simply managing energy balance and body weight. They also include systemic factors which are released into the circulation during exercise and which appear to underlie the myriad of benefits exercise can elicit. It was shown that along with a number of classical cytokines, active tissues also engage in inter-tissue communication via extracellular vesicles (EVs), specifically exosomes and other small EVs, which are able to deliver biomolecules to cells and alter their metabolism. Thus, EVs may play a role in the acute and systemic adaptations that take place during and after physical activity, and may be therapeutically useful in the treatment of a range of diseases, including metabolic disorders such as type 2 diabetes and obesity; and the focus of this review, neurological disorders such as Alzheimer’s disease.

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“…It is known that exercise stimulates brain entrance of circulating IGF-I, which mediates many beneficial exercise actions in the brain (Carro et al, 2000 ; Trejo et al, 2001 ). Indeed, our previous findings indicated that physical exercise activates the EEG, increasing the hippocampal theta rhythm and improving memory in healthy mice, suggesting that the exercise-evoked increase of IGF-I may favor cortical activity and memory processes (Miki Stein et al, 2017 ). In addition, there are also pathological situations in which circulating IGF-signaling is decreased, such as diabetes and Alzheimer’s disease (Torres-Aleman, 2005 ; Fernandez et al, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

Reduced Insulin-Like Growth Factor-I Effects in the Basal Forebrain of Aging Mouse

Zegarra-Valdivia

Chaves-Coira

Sevilla

et al. 2021

Front. Aging Neurosci.

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It is known that aging is frequently accompanied by a decline in cognition. Furthermore, aging is associated with lower serum IGF-I levels that may contribute to this deterioration. We studied the effect of IGF-I in neurons of the horizontal diagonal band of Broca (HDB) of young (≤6 months old) and old (≥20-month-old) mice to determine if changes in the response of these neurons to IGF-I occur along with aging. Local injection of IGF-I in the HDB nucleus increased their neuronal activity and induced fast oscillatory activity in the electrocorticogram (ECoG). Furthermore, IGF-I facilitated tactile responses in the primary somatosensory cortex elicited by air-puffs delivered in the whiskers. These excitatory effects decreased in old mice. Immunohistochemistry showed that cholinergic HDB neurons express IGF-I receptors and that IGF-I injection increased the expression of c-fos in young, but not in old animals. IGF-I increased the activity of optogenetically-identified cholinergic neurons in young animals, suggesting that most of the IGF-I-induced excitatory effects were mediated by activation of these neurons. Effects of aging were partially ameliorated by chronic IGF-I treatment in old mice. The present findings suggest that reduced IGF-I activity in old animals participates in age-associated changes in cortical activity.

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Acute exercise does not modify brain activity and memory performance in APP/PS1 mice

Cited by 20 publications

References 51 publications

Response Facilitation Induced by Insulin-like Growth Factor-I in the Primary Somatosensory Cortex of Mice Was Reduced in Aging

Response Facilitation Induced by Insulin-like Growth Factor-I in the Primary Somatosensory Cortex of Mice Was Reduced in Aging

The Protective Effect of Exercise in Neurodegenerative Diseases: The Potential Role of Extracellular Vesicles

Reduced Insulin-Like Growth Factor-I Effects in the Basal Forebrain of Aging Mouse

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