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These findings suggest that central nervous inflammation may act as a direct potential driver of PEM symptom development, converting peripheral immune and metabolic dysfunction signals into neurofunctional impairments

Author Contributions Conceptualization, J.V

doi: 10.1038/s41590-020-0620-x 208 DongWWuXMaSWangYNalinAPZhuZet al

Transcriptomics and biochemical evidence of trigonelline ameliorating learning and memory decline in the senescence-accelerated mouse prone 8 (SAMP8) model by suppressing proinflammatory cytokines and elevating neurotransmitter release