中国神经再生研究(英文版) ›› 2025, Vol. 20 ›› Issue (12): 3531-3532.doi: 10.4103/NRR.NRR-D-24-00934

• 观点:退行性病与再生 • 上一篇    下一篇

阿尔茨海默病治疗前景:现有疗法和新兴机制的靶向疗法

  

  • 出版日期:2025-12-15 发布日期:2025-03-15

Alzheimer’s disease treatment landscape: current therapies and emerging mechanism-targeted approaches

Eleen Yang, Khaled S. Abd-Elrahman*   

  1. Department of Anesthesiology, Pharmacology and Therapeutics, and Djavad Mowafaghian Center for Brain Health, University of British Columbia, Vancouver, BC, Canada (Yang E, Abd-Elrahman KS) Department of Medical Sciences, College of Medicine and Health Sciences, Khalifa University, Abu Dhabi, United Arab Emirates (Abd-Elrahman KS) Department of Pharmacology and Toxicology, Faculty of Pharmacy, Alexandria University, Alexandria, Egypt (Abd-Elrahman KS)
  • Online:2025-12-15 Published:2025-03-15
  • Contact: Khaled S. Abd-Elrahman, PhD, khaled.abdelrahman@ubc.ca.
  • Supported by:
    KSAE is a Michael Smith Health Research BC funded Health-Professional Investigator. This work was supported by a New Investigator grant from the Alzheimer’s Society of Canada and Alzheimer’s’ disease research grant from Djavad Mowafaghian Centre for Brain Health to KSAE.

摘要: https://orcid.org/0000-0001-9724-1975 (Khaled S. Abd-Elrahman) https://orcid.org/0009-0001-2329-3016 (Eleen Yang)

Abstract: Alzheimer ’s disease (AD) is an age-related neurodegenerative disease that involves a progressive decline in memory, thinking, and learning. AD has been studied rigorously for more than 50 years yet there is a marked lack of progress in pharmacological treatment. The challenges to developing AD therapeutics are rooted in the disease being ill-defined in terms of diagnosis, progression, and etiology. The neuropathological hallmarks of AD are extracellular amyloid-β (Aβ) plaques and intracellular neurofibrillary tangles of hyperphosphorylated tau. Generally, Aβ plaques disrupt neuronal connectivity, while neurofibrillary tangles interfere with intracellular function (Zhang et al., 2023). Therefore, developing innovative strategies to slow the formation or enhance the clearance of these toxic proteins has shown promise in disease-modifying approaches for AD.