Search

Behavioral experiments have demonstrated that long-term physical exercise can be beneficial for learning and memory dysfunction caused by neuroinflammation in Alzheimer's disease (AD). However, the molecular mechanism remains poorly understood due to a lack of sufficient pertinent biochemical evidence. We investigated the potential effect of long-term physical exercise on cognition and hippocampal gene and protein expression changes in a transgenic AD mouse model. Following twenty weeks of treadmill exercise, transgenic AD mice showed improvement in cognitive functions and downregulation of Nod-like receptor protein 3 (NLRP3) (p ​

Abstract Methamphetamine (MA) abuse is recognized as a brain disorder, and physical activity has clear benefits for MA use disorders. The specific mechanisms by which physical activity alleviates MA use disorders are currently not fully understood. Based on this, the present study used untargeted metabolomics using liquid chromatography-mass spectrometry (LC-MS) to analyze the metabolic changes induced by MA in the brains of mice by exercise intervention. It was found that after 2 weeks of treadmill training, aerobic exercise modulated MA-induced brain metabolic disorders, in which 129 metabolites existed that were significantly differentiated in response to MA induction, and 32 metabolites were significantly affected by exercise. These differential metabolites were mainly enriched in glycerophospholipid metabolism, steroid hormone biosynthesis and degradation, and renin-angiotensin system pathways. To our knowledge, this study is the first to use LC-MS to investigate the effects of aerobic exercise on MA-induced brain metabolic profiling. The findings of this study provide new insights into exercise therapy using MA.

Summary: 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.

This study aimed to investigate the effect of long-term aerobic exercise on the metabolism of intestinal contents in APP/PS1 mice was studied using a non-targeted metabolomics technique based on high-performance liquid chromatography-mass spectrometry (HPLC-MS) coupling, providing a theoretical basis for exercise to regulate the metabolism of Alzheimer’s disease (AD) organisms. Three-month-old male C57BL/6JNju mice, six wild-type (NC, n = 6); 12 APP/PS1 double transgenic species in total, were randomly divided into AD model (AM, n = 6) and AD model exercise (AE, n = 6) groups. The mice in the NC group were fed naturally, the mice in the AM group were statically placed on a running platform, and the mice in the AE group received a 20-week long-term moderate intensity running platform exercise intervention. Following the exercise intervention, the cecum contents of the mice in each group were collected and analyzed using the HPLC-MS technique, with those meeting both variable important in projection (VIP)> 1.5 and p < 0.05 being screened as differential metabolites. A total of 32 different metabolites were detected between the AM and NC groups, with 19 up-regulated in the AM group such as phosphatidic acid (PA) (18:4(6Z,9Z,12Z,15Z)/21:0) and 13 down-regulated in the AM group, such as 4,8-dimethylnonanoyl, compared to the NC group; 98 different metabolites were found between the AM and AE groups, 41 of which were upregulated such as Lyso phosphatidylcholine (LysoPC) and 57 of which were downregulated compared to the AM group such as Phosphatidylinositol (PI). The regulation of linoleic acid metabolism, glycerophospholipid metabolism, bile secretion, phenylalanine metabolism, and other pathways was predominantly regulated by nine metabolites, which were subsequently identified as indicators of exercise intervention to enhance metabolism in AD mice. The metabolomic technique can identify the metabolic problems of intestinal contents in AD mice and initially screen the biomarkers of exercise to improve the metabolic disorders in AD. These findings can help us better understand the impact of aerobic exercise on AD metabolism.

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.

This study aimed to investigate the changes in intestinal homeostasis and metabolism in mice after methamphetamine (MA) administration and exercise intervention. In this study, male C57BL/B6J mice were selected to establish a model of methamphetamine-induced addiction, and the gut microbiota composition, short-chain fatty acids (SCFAs), and amino acid levels were assessed by 16S rRNA, liquid chromatography–tandem mass spectrometry, and gas chromatography–tandem mass spectrometry, respectively. The results showed that 23 dominant microbiota, 12 amino acids, and 1 SCFA were remarkably higher and 9 amino acids and 6 SCFAs were remarkably lower in the exercise model group than in the control group. Among the top 10 markers with opposite trends between the exercise intervention group and model group, the differential microbiomes included Oscillibacter, Alloprevotella, Colidextribacter, Faecalibaculum, Uncultured, Muribaculaceae, and Negativibacillus; amino acids included proline; and SCFAs included isovaleric acid and pentanoic acid. Proline was negatively correlated with Negativibacillus and positively correlated with pentanoic acid. The results suggested that moderate-intensity aerobic exercise may modulate changes in the composition of the gut microbiota and the levels of amino acids and SCFAs induced by MA administration.