Neural Regeneration Research ›› 2026, Vol. 21 ›› Issue (3): 1126-1127.doi: 10.4103/NRR.NRR-D-24-01591

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Dysregulated insulin signaling and inflammation contribute to the pathogenesis of Alzheimer’s disease: From animal models to human cells

Marcus Elo Rytter, Cecilie Amalie Brøgger Svane, Joachim Størling* , Wenqiang Chen*   

  1. Steno Diabetes Center Copenhagen, Herlev, Denmark (Rytter ME, Svane CAB, Størling J, Chen W) Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark (Størling J) Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA (Chen W)
  • Online:2026-03-15 Published:2025-07-04
  • Contact: Joachim Størling, PhD, joachim.stoerling@regionh.dk; Wenqiang Chen, PhD, wenqiang.chen@joslin.harvard.edu.
  • Supported by:
    This work was supported by grants from NIH T32 (DK007260, to WC), and the Steno North American Fellowship awarded by the Novo Nordisk Foundation (NNF23OC0087108, to WC).

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Abstract: The shared links between Alzheimer’s disease and type 2 diabetes mellitus: Alzheimer’s disease (AD) and type 2 diabetes mellitus (T2DM) are two prevalent conditions that come with substantial daily struggles. Emerging evidence highlights that these diseases share similar pathophysiological features, including insulin resistance and chronic inflammation, which contribute to their rapid progression (Chen et al., 2022). Insulin resistance, a hallmark of T2DM, has been suggested to exacerbate neurodegeneration in AD. Similarly, chronic low-grade inflammation in T2DM parallels with neuroinflammation, which is observed in AD, suggesting overlapping pathophysiological mechanisms in T2DM and AD.