Trying to understand how exercise can help prevent Alzheimer’s disease is like unraveling a complex puzzle. In this captivating study, scientists targeted a specific mechanism called necroptosis, which is an important manifestation of Alzheimer’s. They found that exercise has the power to inhibit necroptosis of neuronal cells, offering a potential explanation for its protective effects against the disease. Furthermore, researchers developed a new logistic regression-based model for predicting AD risk, providing a valuable tool for exercise prescriptions. The model showed exceptional predictive power, with an impressive AUC value of 0.979. On top of that, they discovered that exercise upregulates a specific miRNA called miR-215-5p, which can potentially prevent the expressions of key genes associated with Alzheimer’s pathology. By identifying CEBPB and GATA6 as putative transcriptional regulators of miR-215, the researchers shed light on the intricate control mechanisms within skeletal muscle cells. These findings suggest a fascinating negative feedback loop that helps maintain exosomal homeostasis. To dive deeper into this exciting research and learn about the connection between exercise and Alzheimer’s, check out the full article!

Exercise is crucial for preventing Alzheimer’s disease (AD), although the exact underlying mechanism remains unclear. The construction of an accurate AD risk prediction model is beneficial as it can provide a theoretical basis for preventive exercise prescription. In recent years, necroptosis has been confirmed as an important manifestation of AD, and exercise is known to inhibit necroptosis of neuronal cells. In this study, we extracted 67 necroptosis-related genes and 32 necroptosis-related lncRNAs and screened for key predictive AD risk genes through a random forest analysis. Based on the neural network Prediction model, we constructed a new logistic regression-based AD risk prediction model in order to provide a visual basis for the formulation of exercise prescription. The prediction model had an area under the curve (AUC) value of 0.979, indicative of strong predictive power and a robust clinical application prospect. In the exercise group, the expression of exosomal miR-215-5p was found to be upregulated; miR-215-5p could potentially inhibit the expressions of IDH1, BCL2L11, and SIRT1. The single-cell SCENIC assay was used to identify key transcriptional regulators in skeletal muscle. Among them, CEBPB and GATA6 were identified as putative transcriptional regulators of miR-215. After “skeletal muscle removal of load,” the expressions of CEBPB and GATA6 increased substantially, which in turn led to the elevation of miR-215 expression, thereby suggesting a putative mechanism for negative feedback regulation of exosomal homeostasis.

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