Postnatal high-protein diet improves learning and memory in premature rats via activation of mTOR signaling

Su, Zhiwen; Liao, Junlin; Zhang, Hui; Zhang, Tao; Wu, Fan; Tian, Xiaohua; Zhang, Feitong; Sun, Weiwen; Cui, Qiliang

doi:10.1016/j.brainres.2015.01.052

Cited by 11 publications

(7 citation statements)

References 34 publications

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“…Cognitive dysfunction is the most typical outcome of abnormal neural development in premature infants [49,50]. A study on premature rats suggests that this effect may be due to suppressed mTOR signaling in the hippocampus [51]. Experimental upregulation of mTOR signaling promotes retinal ganglion cell survival and axon regeneration after optic nerve crush injury [52,53].…”

Section: Discussionmentioning

confidence: 99%

Suppression of AMD-Like Pathology by Mitochondria-Targeted Antioxidant SkQ1 Is Associated with a Decrease in the Accumulation of Amyloid β and in mTOR Activity

et al. 2019

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Age-related macular degeneration (AMD) is a major cause of irreversible visual impairment and blindness in developed countries, and the molecular pathogenesis of AMD is poorly understood. Recent studies strongly indicate that amyloid β (Aβ) accumulation —found in the brain and a defining feature of Alzheimer’s disease—also forms in the retina in both Alzheimer’s disease and AMD. The reason why highly neurotoxic proteins of consistently aggregate in the aging retina, and to what extent they contribute to AMD, remains to be fully addressed. Nonetheless, the hypothesis that Aβ is a therapeutic target in AMD is debated. Here, we showed that long-term treatment with SkQ1 (250 nmol/[kg body weight] daily from the age of 1.5 to 22 months) suppressed the development of AMD-like pathology in senescence-accelerated OXYS rats by reducing the level of Aβ and suppressing the activity of mTOR in the retina. Inhibition of mTOR signaling activity, which plays key roles in aging and age-related diseases, can be considered a new mechanism of the prophylactic effect of SkQ1. It seems probable that dietary supplementation with mitochondria-targeted antioxidant SkQ1 can be a good prevention strategy to maintain eye health and possibly a treatment of AMD.

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Section: Discussionmentioning

confidence: 99%

Suppression of AMD-Like Pathology by Mitochondria-Targeted Antioxidant SkQ1 Is Associated with a Decrease in the Accumulation of Amyloid β and in mTOR Activity

et al. 2019

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“…Combined with prior reports of increased mTOR signaling in peripheral tissues following exercise [80, 81], these data suggest that mTOR signaling could be a fundamental and ubiquitous cellular target of physical activity. Given the emerging data supporting a role for mTOR in neural plasticity [27, 82], cognitive function [24–26] and emotional regulation [36, 40], increases in mTOR signaling following exercise could contribute to the broad beneficial impact of exercise on brain health, cognition, and emotional behavior.…”

Section: Discussionmentioning

confidence: 99%

Exercise increases mTOR signaling in brain regions involved in cognition and emotional behavior

Lloyd

Hake

Ishiwata

et al. 2017

Behavioural Brain Research

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Exercise can enhance learning and memory and produce resistance against stress-related psychiatric disorders such as depression and anxiety. In rats, these beneficial effects of exercise occur regardless of exercise controllability: both voluntary and forced wheel running produce stress-protective effects. The mechanisms underlying these beneficial effects of exercise remain unknown. The mammalian target of rapamycin (mTOR) is a translation regulator important for cell growth, proliferation, and survival. mTOR has been implicated in enhancing learning and memory as well as antidepressant effects. Moreover, mTOR is sensitive to exercise signals such as metabolic factors. The effects of exercise on mTOR signaling, however, remain unknown. The goal of the present study was to test the hypothesis that exercise, regardless of controllability, increases levels of phosphorylated mTOR (p-mTOR) in brain regions important for learning and emotional behavior. Rats were exposed to 6 weeks of either sedentary (locked wheel), voluntary, or forced wheel running conditions. At 6 weeks, rats were sacrificed during peak running and levels of p-mTOR were measured using immunohistochemistry. Overall, both voluntary and forced exercise increased p-mTOR-positive neurons in the medial prefrontal cortex, striatum, hippocampus, hypothalamus, and amygdala compared to locked wheel controls. Exercise, regardless of controllability, also increased numbers of p-mTOR-positive glia in the striatum, hippocampus, and amygdala. For both neurons and glia, the largest increase in p-mTOR positive cells was observed after voluntary running, with forced exercise causing a more modest increase. Interestingly, voluntary exercise preferentially increased p-mTOR in astrocytes (GFAP+), while forced running increased p-mTOR in microglia (CD11+) in the inferior dentate gyrus. Results suggest that mTOR signaling is sensitive to exercise, but subtle differences exist depending on exercise controllability. Increases in mTOR signaling could contribute to the beneficial effects of exercise on cognitive function and mental health.

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“…Most importantly, Su et al (2015) showed that the activation of mTOR pathway components was lower in the hippocampus of premature rats relative to full-term rats, and this was associated with poorer learning and memory performance. They showed that long-term consumption of a protein-rich diet can restore the impairment in learning and memory in pre-term rats via upregulation of mTOR-S6K1 signaling.…”

Section: Mtor In the Adult Cnsmentioning

confidence: 99%

Mammalian Target of Rapamycin: Its Role in Early Neural Development and in Adult and Aged Brain Function

Garza-Lombó

Gonsebatt

2016

Front. Cell. Neurosci.

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The kinase mammalian target of rapamycin (mTOR) integrates signals triggered by energy, stress, oxygen levels, and growth factors. It regulates ribosome biogenesis, mRNA translation, nutrient metabolism, and autophagy. mTOR participates in various functions of the brain, such as synaptic plasticity, adult neurogenesis, memory, and learning. mTOR is present during early neural development and participates in axon and dendrite development, neuron differentiation, and gliogenesis, among other processes. Furthermore, mTOR has been shown to modulate lifespan in multiple organisms. This protein is an important energy sensor that is present throughout our lifetime its role must be precisely described in order to develop therapeutic strategies and prevent diseases of the central nervous system. The aim of this review is to present our current understanding of the functions of mTOR in neural development, the adult brain and aging.

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Postnatal high-protein diet improves learning and memory in premature rats via activation of mTOR signaling

Cited by 11 publications

References 34 publications

Suppression of AMD-Like Pathology by Mitochondria-Targeted Antioxidant SkQ1 Is Associated with a Decrease in the Accumulation of Amyloid β and in mTOR Activity

Suppression of AMD-Like Pathology by Mitochondria-Targeted Antioxidant SkQ1 Is Associated with a Decrease in the Accumulation of Amyloid β and in mTOR Activity

Exercise increases mTOR signaling in brain regions involved in cognition and emotional behavior

Mammalian Target of Rapamycin: Its Role in Early Neural Development and in Adult and Aged Brain Function

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