中国神经再生研究(英文版) ›› 2026, Vol. 21 ›› Issue (10): 4880-4881.doi: 10.4103/NRR.NRR-D-25-00709

• 观点:退行性病与再生 • 上一篇    下一篇

脂质组改变是阿尔茨海默病的标志和治疗靶点

  

  • 出版日期:2026-10-15 发布日期:2026-06-13

Lipidome alteration as a hallmark and therapeutic target in Alzheimer’s disease

Sijia He, Xianlin Han*   

  1. Barshop Institute for Longevity and Aging Studies, University of Texas Health San Antonio, San Antonio, TX, USA (He S, Han X) 
    Department of Cellular and Integrative Physiology, University of Texas Health San Antonio, San Antonio, TX, USA (He S) 
    Division of Diabetes, Department of Medicine, University of Texas Health San Antonio, San Antonio, TX, USA (Han X)
  • Online:2026-10-15 Published:2026-06-13
  • Contact: Xianlin Han, PhD, hanx@uthscsa.edu.
  • Supported by:
    This work was supported by National Institute on Aging grants R01AG061872 (to XH), RF1AG061729 (to XH), R01AG085545 (to XH), T32AG021890 (to SH), P30AG013319, and P30AG044271, the Methodist Hospital Foundation (to XH), the Cure Alzheimer’s Fund (to XH), the Owen Foundation (to XH), the American Federation for Aging Research (to SH), and the Owen Foundation (to SH).

摘要: https://orcid.org/0000-0002-8615-2413 (Xianlin Han)

Abstract: Alzheimer ’s disease (AD) is a progressive neurodegenerative disorder marked by cognitive decline and memory loss. Its well-established pathological features include the presence of extracellular amyloid-beta (Aβ) plaques, intracellular tau-containing neurofibrillary tangles, and neuroinflammation (He et al., 2025). While AD research over the past few decades has focused mainly on genetic and protein-centric mechanisms, a growing body of evidence points to lipids as a critical, yet previously underappreciated dimension of AD pathology. Recent advances in lipidomics emphasize that lipid dysregulation is not merely a secondary disease phenomenon, but rather a central component, and potentially a driving force of AD progression. This perspective article highlights altered lipid metabolism as both a hallmark and a promising therapeutic target for AD.