Calorie restriction ameliorates neurodegenerative phenotypes in forebrain-specific presenilin-1 and presenilin-2 double knockout mice

Wu, Pu; Shen, Qian; Shen, Dong; Xu, Zhiliang; Tsien, Joe Z.; Hu, Yinghe

doi:10.1016/j.neurobiolaging.2007.03.028

Cited by 100 publications

(65 citation statements)

References 40 publications

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“…We thus compiled unbiased compatible gene lists from a common population (genes on the MM5 array to which Ensembl identifiers could be assigned) for genes found to be responsive to DR and found to show ageing-related changes in methylation status. Genes regulated by DR, leading to a change in abundance of the corresponding mRNA, were identified from published studies involving DR in mice (Lee et al 2002;Higami et al 2004;Massaro et al 2004;Tsuchiya et al 2004;Han and Hickey 2005;Dhahbi et al 2006;Fu et al 2006;Selman et al 2006;Sharov et al 2008;Swindell 2008;Wu et al 2008). We accepted for each published study the authors' list of regulated genes and used data regardless of tissue investigated.…”

Section: Resultsmentioning

confidence: 99%

Effects of Sirt1 on DNA methylation and expression of genes affected by dietary restriction

Ions

Wakeling

Bosomworth

et al. 2012

AGE

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Changes in DNA methylation across the life course may contribute to the ageing process. We hypothesised that some effects of dietary restriction to extend lifespan and/or mitigate against features of ageing result from changes in DNA methylation, so we determined if genes that respond to dietary restriction also show age-related changes in DNA methylation. In support of our hypothesis, the intersection of lists of genes compiled from published sources that (1) were differentially expressed in response to dietary restriction and (2) showed altered methylation with increased age was greater than expected. We also hypothesised that some effects of Sirt1, which may play a pivotal role in beneficial effects of dietary restriction, are mediated through DNA methylation. We thus measured effects of Sirt1 overexpression and knockdown in a human cell line on DNA methylation and expression of a panel of eight genes that respond to dietary restriction and show altered methylation with age. Six genes were affected at the level of DNA methylation, and for six expressions were affected. In further support of our hypothesis, we observed by DNA microarray analysis that genes showing differential expression in response to Sirt1 knockdown were over-represented in the complied list of genes that respond to dietary restriction. The findings reveal that

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Section: Resultsmentioning

confidence: 99%

Effects of Sirt1 on DNA methylation and expression of genes affected by dietary restriction

Ions

Wakeling

Bosomworth

et al. 2012

AGE

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“…14) However, the effect of calorie restriction on cognition in MetS is still controversial. 12,13,19) In hypertensive (not MetS) model rats, we also could not determine the benefit of calorie restriction on cognition. 20) With respect to the discrepancy between the benefit of calorie restriction on cognition in the hypertensive or MetS model, we should consider that insulin resistance and obesity worsen cognition.…”

Section: Discussionmentioning

confidence: 99%

“…Not only pharmacological therapy but also exercise training [9][10][11] and calorie restriction 12,13) have been suggested to protect against cognitive decline. The benefits of calorie restriction on metabolic syndrome have been already established via improvement of insulin-resistance.…”

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confidence: 99%

Calorie Restriction Improves Cognitive Decline via Up-Regulation of Brain-Derived Neurotrophic Factor

et al. 2015

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SummaryIn metabolic syndrome (MetS), previous studies have suggested that cognitive decline is worsened. Among the factors associated with cognition, decreased brain-derived neurotrophic factor (BDNF) in the hippocampus causes cognitive decline. We previously reported that exercise training with calorie restriction yielded protection against cognitive decline via BDNF in the hippocampus of hypertensive rats. The aim of the present study was to determine whether or not calorie restriction results in protection against cognitive decline via BDNF and its receptor tropomyosin-related kinase B (TrkB) in the hippocampus of MetS model rats. We divided dietary-induced obesity-prone and hypertensive rats (OP), as metabolic syndrome model rats, into three groups, fed with a high fat diet (HF), treated with calorie restriction (CR) plus vehicle, and treated with CR and ANA-12 (a TrkB antagonist) (CR+A). After treatment for 28 days, body weight, insulin, fasting blood glucose, adiponectin, systolic blood pressure, and oxidative stress in the hippocampus were significantly lower, and BDNF expression in the hippocampus was significantly higher in CR and CR+A than in HF. Cognitive performance determined by the Morris water maze test was significantly higher in CR than in HF, whereas the benefit was attenuated in CR+A. In conclusion, calorie restriction protects against cognitive decline via up-regulation of BDNF/TrkB through an antioxidant effect in the hippocampus of dietary-induced obesity rats. (Int Heart J 2015; 56: 110-115) Key words: Metabolic syndrome, Cognition O ne of the important types of organ damage in metabolic syndrome (MetS) is cognitive decline. 1) MetS-associated factors are linked to volume losses in the hippocampus, and MetS negatively impacts cognition by impaired vascular reactivity, neuro-inflammation, oxidative stress, and abnormal brain lipid metabolism.1) Among the factors associated with cognition, brain-derived neurotrophic factor (BDNF) and its receptor tropomyosin-related kinase B (TrkB) are known to be involved in the protective mechanisms against stress and cell death as an antioxidant.2-6) Systemic oxidative stress and/or antioxidant deficiency cause cognitive decline, 7) and oxidative stress in the hippocampus in particular impairs cognitive function. 8) However, it has not been clarified whether BDNF/TrkB in the hippocampus of metabolic syndrome patients is impaired or not.Not only pharmacological therapy but also exercise training 9-11) and calorie restriction 12,13) have been suggested to protect against cognitive decline. The benefits of calorie restriction on metabolic syndrome have been already established via improvement of insulin-resistance. [13][14][15][16][17][18] However, in a previous clinical study, calorie restriction and/or exercise training did not protect against cognitive decline. 19) We previously demonstrated that exercise training plus calorie restriction causes synergistic protection against cognitive decline via up-regulation of BDNF in the hippocampus of stroke-pron...

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“…CR diets or intermittent fasting can rescue the cognitive deficits in the transgenic mouse models of AD [8] . The effect is associated with alleviated hippocampal atrophy, β-amyloid burden and hyperphosphorylation of tau protein in the brain [8,9] . In a study of model of accelerated aging, CR attenuated the deficits of learning and memory in middle-aged senescence-accelerated mouse strain P 8 (SAMP8) mice in a passive avoidance task [10] .…”

Section: Calorie Restrictionmentioning

confidence: 99%

“…During normal brain aging and AD, a declined expression of brain-derived neurotrophic factor and its receptor tryosine receptor kinase B has been found, and this decline is correlated with impaired cognitive functions and decreased dendritic spine density in hippocampus [16] . What's more, evidence from genetic studies has demonstrated that after a 4-month CR, the genes related to neurogenesis and synaptic plasticity become upregulated, while the genes associated with inflammation become downregulated in the hippocampus of transgenic AD mice [9] .…”

Section: Calorie Restrictionmentioning

confidence: 99%

Fight against Glucose Rescues Age-Related Cognitive Decline

Tong

Chen

2016

Neurosci Commun

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Aging is commonly associated with dysfunctions of various systems, especially the cognitive decline that seriously diminishes the independence and life quality of old individuals. Exploring the approaches for maintaining a healthy brain is now a critical public health concern. Calorie restriction (CR) has been known to extend longevity, promote metabolic health, and delay the progress of aging and the risk of age-related diseases, such as type 2 diabetes and Alzheimer's disease (AD). Studies have shown that CR improves the insulin sensitivity. Moreover, defected insulin signaling in individuals with or without diabetes is related to a higher risk of age-related cognitive deficits or AD. Evidences suggest that treatment of diabetes mimics the activity of CR, modulating the metabolism of glucose and lipid and the function of insulin system, thus may has the anti-aging potential. In this paper, we reviewed the laboratory experiment and clinical data that focused on the protective role of CR, and that investigated the effect of several types of common agents for diabetes treatment on aging or cognitive ability. The progress in recent years inspires researchers to explore the mechanisms of age-related cognitive decline, and search for safe and effective therapeutic strategies. In the future, more high-quality studies are required to optimize the application of CR or diabetes therapies on the prevention or treatment of brain aging.

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Calorie restriction ameliorates neurodegenerative phenotypes in forebrain-specific presenilin-1 and presenilin-2 double knockout mice

Cited by 100 publications

References 40 publications

Effects of Sirt1 on DNA methylation and expression of genes affected by dietary restriction

Effects of Sirt1 on DNA methylation and expression of genes affected by dietary restriction

Calorie Restriction Improves Cognitive Decline via Up-Regulation of Brain-Derived Neurotrophic Factor

Fight against Glucose Rescues Age-Related Cognitive Decline

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