中国神经再生研究(英文版) ›› 2026, Vol. 21 ›› Issue (2): 683-684.doi: 10.4103/NRR.NRR-D-24-01227

• 观点:退行性病与再生 • 上一篇    下一篇

阿尔茨海默病突触功能障碍的生物标志物

  

  • 出版日期:2026-02-15 发布日期:2025-05-23

Biomarkers for synaptic dysfunction in Alzheimer’s disease

Ruiqing Ni*   

  1. Institute for Regenerative Medicine, University of Zurich; Institute for Biomedical Engineering, ETH Zurich and University of Zurich, Zurich, Switzerland Department of Nuclear Medicine, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland
  • Online:2026-02-15 Published:2025-05-23
  • Contact: Ruiqing Ni, PhD, ruiqing.ni@uzh.ch.
  • Supported by:
    This work was supported by Swiss Center for Applied Human Toxicology (SCAHT AP22-01) (to RN).

摘要: https://orcid.org/0000-0002-0793-2113 (Ruiqing Ni)

Abstract: Alzheimer’s disease (AD) is the most common cause of dementia, characterized by progressive cognitive decline, and affects over 55 million people worldwide. AD is pathological featured by the aberrant accumulation of amyloid-β plaques, neurofibrillary tangles formed by hyperphosphorylated tau, synaptic loss, and dysfunction of neurotransmitter systems. Evidence from in vivo and autopsy studies has consistently shown that synaptic dysfunction and loss are strongly correlated with cognitive decline in AD, particularly in brain regions such as the hippocampus and cortex, which are critical for memory formation and processing. This perspective highlights recent histopathological findings related to synaptic dysfunction in AD, advancements in the development of imaging and fluid-based biomarkers for synaptic loss, and future studies.