AI Article Synopsis

  • Exercise is linked to better cognitive health, particularly in the hippocampus, which is crucial for learning and memory.
  • Research shows that exercise improves neurogenesis (the creation of new neurons) and synaptic plasticity, but the specific molecular mechanisms are still unclear.
  • A new study provides a detailed dataset from the mouse hippocampus after 4 weeks of voluntary exercise, revealing that exercise speeds up the maturation of certain neurons and alters key signaling pathways, potentially guiding future interventions to enhance cognitive health.

Article Abstract

Exercise has been recognized as a beneficial factor for cognitive health, particularly in relation to the hippocampus, a vital brain region responsible for learning and memory. Previous research has demonstrated that exercise-mediated improvement of learning and memory in humans and rodents correlates with increased adult neurogenesis and processes related to enhanced synaptic plasticity. Nevertheless, the underlying molecular mechanisms are not fully understood. With the aim to further elucidate these mechanisms, we provide a comprehensive dataset of the mouse hippocampal transcriptome at the single-cell level after 4 weeks of voluntary wheel-running. Our analysis provides a number of interesting observations. For example, the results suggest that exercise affects adult neurogenesis by accelerating the maturation of a subpopulation of Prdm16-expressing neurons. Moreover, we uncover the existence of an intricate crosstalk among multiple vital signaling pathways such as NF-κB, Wnt/β-catenin, Notch, and retinoic acid (RA) pathways altered upon exercise in a specific cluster of excitatory neurons within the Cornu Ammonis (CA) region of the hippocampus. In conclusion, our study provides an important resource dataset and sheds further light on the molecular changes induced by exercise in the hippocampus. These findings have implications for developing targeted interventions aimed at optimizing cognitive health and preventing age-related cognitive decline.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11249425PMC
http://dx.doi.org/10.1007/s12035-023-03869-9DOI Listing

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