中国神经再生研究(英文版) ›› 2020, Vol. 15 ›› Issue (6): 1030-1032.doi: 10.4103/1673-5374.270306

• 观点:退行性病与再生 • 上一篇    下一篇

阿尔茨海默病中的血管功能障碍 - 疾病进展的生物标志物和潜在的治疗靶点

  

  • 出版日期:2020-06-15 发布日期:2020-07-01

Vascular dysfunction in Alzheimer’s disease: a biomarker of disease progression and a potential therapeutic target

Karan Govindpani, Chitra Vinnakota, Henry J. Waldvogel, Richard L. Faull, Andrea Kwakowsky   

  1. Centre for Brain Research, Department of Anatomy and Medical Imaging, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand
  • Online:2020-06-15 Published:2020-07-01
  • Contact: Andrea Kwakowsky, PhD,a.kwakowsky@auckland.ac.nz.

摘要: orcid: 0000-0002-3801-4956 (Andrea Kwakowsky)

Abstract: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the predominant form of dementia. Since its initial description by Alois Alzheimer in 1906, several advances have been made in our understanding of the progression of the disease and its clinical consequences, yet the underlying etiology remains contentious. Given the stereotyped patterns of cortical and hippocampal neuronal loss and the progressive degeneration of key neurotransmitter pathways, research has traditionally been focused on factors affecting neuronal viability, including the contribution of glial dysfunction to neuronal degeneration. From a clinical perspective, the fruits of this work have been underwhelming. Key pathological markers of the disease, including β-amyloid (Aβ) plaque formation and tau hyperphosphorylation, have yielded no effective therapies, highlighted by the recent discontinuations of several high profile Aβ immunotherapy trials. The few current symptomatic therapies for AD are predicated on the amelioration of cholinergic or glutamatergic dysfunction. Aside from underscoring the inadequacy of current therapeutic approaches, this also points to the importance of alternative contributors to AD pathogenesis. In recent years, there has been a growing appreciation for the multimodal and multifactorial nature of the condition; the case for combinatorial therapies is thus strong.