中国神经再生研究(英文版) ›› 2025, Vol. 20 ›› Issue (1): 203-204.doi: 10.4103/NRR.NRR-D-23-02093

• 观点:退行性病与再生 • 上一篇    下一篇

纤维蛋白原在阿尔茨海默病脑血管异常与淋巴功能紊乱之间的潜在联系

  

  • 出版日期:2025-01-15 发布日期:2025-01-15

Fibrinogen’s potential role in connecting cerebrovascular abnormalities with glymphatic dysfunction in Alzheimer’s disease

Vishal Singh#, Arnab Choudhury#, Hyung Jin Ahn*   

  1. Department of Pharmacology, Physiology and Neurosciences, Rutgers-New Jersey Medical School, Newark, NJ, USA (Singh V, Choudhury A, Ahn HJ) 
    Brain Health Institute, Rutgers University, Piscataway, NJ, USA (Ahn HJ)
  • Online:2025-01-15 Published:2025-01-15
  • Contact: Hyung Jin Ahn, PhD, hyungjin.ahn@rutgers.edu.
  • Supported by:
    This work was supported by the National Institute of Health NS104386 (to HJA) and AG078245 (to HJA).

摘要: https://orcid.org/0000-0003-0715-7222 (Hyung Jin Ahn) 

Abstract: Alzheimer’s disease (AD) stands out as the primary manifestation of age-related dementia, portraying a chronic neurodegenerative disorder distinguished by the accumulation of fibrillar amyloid-β (Aβ) plaques and neurofibrillary tangles of hyperphosphorylated tau. However, from a clinical standpoint, AD presents itself as a complex condition with a spectrum of dysfunctions rather than a singular pathological mechanism. An often-overlooked aspect of the disease is the presence of extensive cerebrovascular abnormalities, given that the majority of AD patients experience altered cerebral blood flow, damaged vasculature, increased microinfarcts and microhemorrhages. Animal models of AD further support this observation, showing cerebrovascular dysfunction such as impaired cerebral blood flow and altered cerebrovascular reactivity (Tataryn et al., 2021; Gareau et al., 2023).