Neural Regeneration Research ›› 2025, Vol. 20 ›› Issue (6): 1711-1712.doi: 10.4103/NRR.NRR-D-24-00351

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Sleep as a window to understand and regulate Alzheimer’s disease: emerging roles of thalamic reticular nucleus

Haoqi Sun, Shiqian Shen, Robert J. Thomas, M. Brandon Westover, Can Zhang*   

  1. Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA (Sun H, Westover MB) Center for Translational Pain Research, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA (Shen S) Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA (Thomas RJ) Genetics and Aging Research Unit, McCance Center for Brain Health, Mass General Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA (Zhang C)
  • Online:2025-06-15 Published:2024-11-12
  • Contact: Can Zhang, MD, PhD, zhang.can@mgh.harvard.edu.
  • Supported by:
    This work was supported by the Massachusetts General Hospital Scientific Projects to Accelerate Research and Collaboration (SPARC) award and Cure Alzheimer’s Fund (to CZ); the National Institutes of Health (NIH), including R01NS102190, RF1NS120947, and R01HL161253 (to MBW); RF1NS120947 (to RJT). Dr. Westover is the co-founder of Beacon Biosignals, which is not involved in any part of this article. Dr. Thomas has a patent for an ECG/ PPG sleep spectrogram licensed by the Beth Israel Deaconess Medical Center to MyCardio, LLC. He consults for GLG Councils and Guidepoint Global. Other authors have nothing to disclose.

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Abstract: Introduction: Alzheimer ’s disease (AD) is a common neurodegenerative disorder and the primary cause of dementia. Considerable evidence supports the “amyloid hypothesis,” stating that the pathogenesis of AD is primarily caused by the deposition of amyloid-β (Aβ), which drives tau phosphorylation, neuroinflammation, and neurodegeneration in the brain. The amyloid hypothesis is strengthened by the significant and moderate benefit of lecanemab, a humanized antibody through an anti-amyloid mechanism, showing slowed clinical decline (van Dyck et al., 2023). The recent positive results of anti-amyloid trials have brought back focus on the amyloid hypothesis through biochemical, genetic, and pharmacological approaches (Zhang, 2023). As a complex disease, AD neuropathology and risk are heterogeneous and regulated by aging, genetics, and sex, in combination with other risk-modifying factors. Among the risk factors of AD, sleep disturbance is an important factor that may occur early in AD and last throughout the disease.