Time-resolved map of serum metabolome profiling in D-galactose-induced aging rats with exercise intervention.

Exercise, an intervention with wide-ranging effects on the whole body, has been shown to delay aging. Due to aging and exercise as modulator of metabolism, a picture of how exercise delayed D-galactose (D-gal)-induced aging in a time-resolved manner was presented in this paper. The mapping of molecular changes in response to exercise has become increasingly accessible with the development of omics techniques. To explore the dynamic changes during exercise, the serum of rats and D-gal-induced aging rats before, during, and after exercise was analyzed by untargeted metabolomics. The variation of metabolites was monitored to reveal the specific response to D-gal-induced senescence and exercise in multiple pathways, especially the basal amino acid metabolism, including glycine serine and threonine metabolism, cysteine and methionine metabolism, and tryptophan metabolism. The homeostasis was disturbed by D-gal and maintained by exercise. The paper was expected to provide a theoretical basis for the study of anti-aging exercise.

Visualization analysis of exercise intervention on Alzheimer disease based on bibliometrics: Trends, hotspots and topics.

BACKGROUND: As the challenges of an aging society continue to escalate, Alzheimer disease (AD) has emerged as a significant health, social, and public concern, garnering substantial attention. Exercise, as a safe, effective, and cost-efficient approach with the potential to mitigate brain aging, has garnered considerable interest. Nevertheless, there has been a limited research investigating the current trends, hotspots, and topics of exercise on AD. METHODS: The literature spanning from 2013 to 2022 was obtained from the Web of Science database, and CiteSpace VI was employed to conduct an analysis encompassing fundamental data, keywords, and co-citation analysis. RESULTS: A total of 9372 publications were included in the analysis. The annual number of publications has exhibited a gradual increase. The United States and China made significant contributions, with England showing higher citation rates and greater academic influence. The Journal of Alzheimers Disease, Neurosciences Neurology, Liu-Ambrose, Teresa represents the most published journal, discipline, and author, respectively. The research trends can be summarized as exploring functional changes and potential mechanisms related to exercise impact on AD. The hotspots in the research include the intersection of AD and diabetes mellitus, as well as the underlying effects induced by exercise. The topics of interest revolve around the application of emerging technologies in the context of exercise and AD. CONCLUSION: This bibliometric analysis has identified relevant trends, hotspots, and topics within the exercise intervention on AD. It offers a comprehensive overview that can equip researchers with valuable insights for future exploration and assist scholars in charting research trajectories in related domains.

Bioinformatics Analysis and Experimental Verification of Exercise for Aging Mice in Different Brain Regions Based on Transcriptome Sequencing.

PURPOSE: Physical exercise mitigates the effects of aging and cognitive decline. However, the precise neurobiological mechanisms underlying this phenomenon remain unclear. The primary aim of this study was to investigate the protective effect of exercise on age-related memory deficits in the prefrontal cortex (PFC) and hippocampus using bioinformatic analysis and biochemical verification. METHODS: Young and aging mice were subjected to natural feeding or treadmill exercise (12 m/min, 8 weeks). Cognitive function was accessed using the Barnes maze and novel object recognition. Bioinformatic analysis was performed to identify co-expressed genes in different groups and brain regions. The selected genes and pathways were validated using RT-qPCR. RESULTS: Regular exercise significantly ameliorated age-related cognitive deficits. Four up-regulated targets (Ifi27l2a, Irf7, Oas1b, Ifit1) and one down-regulation (Septin2) were reversed by exercise, demonstrating the underlying mechanisms of cognitive functions induced by aging with exercise in the hippocampus and PFC. The Gene Ontology terms and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses indicated that the NOD-like receptor signaling pathway was inhibited in the neuroinflammation effects of exercise in aging mice in both brain regions. CONCLUSION: Exercise enhances age-related learning and memory deficits. This beneficial effect may be attributed to the changes in five up/down-regulated genes and the NOD-like receptor signaling pathway in both the hippocampus and PFC. These findings establish the modulation of neuroinflammation as a pivotal molecular mechanism supporting exercise intervention in the brain aging process.