中国神经再生研究(英文版) ›› 2025, Vol. 20 ›› Issue (11): 3219-3220.doi: 10.4103/NRR.NRR-D-24-00699

• 观点:退行性病与再生 • 上一篇    下一篇

错误折叠的淀粉样β蛋白构象变体(菌株)是阿尔茨海默病神经病理学的驱动因素

  

  • 出版日期:2025-11-15 发布日期:2025-02-23

Misfolded amyloid-beta conformational variants (strains) as drivers of Alzheimer’s disease neuropathology

Salvatore Saieva, Rodrigo Morales*   

  1. Department of Neurology, The University of Texas Health Science Center at Houston, Houston, TX, USA (Saieva S, Morales R) Centro Integrativo de Biologia y Quimica Aplicada (CIBQA), Universidad Bernardo O’Higgins, Santiago, Chile (Morales R)
  • Online:2025-11-15 Published:2025-02-23
  • Contact: Rodrigo Morales, PhD, Rodrigo.MoralesLoyola@uth.tmc.edu.
  • Supported by:
    This work was supported by a grant from NIH (R01AI132695) to RM.

摘要: https://orcid.org/0000-0001-7766-5770 (Rodrigo Morales)

Abstract: Pathological and clinical variability in Alzheimer’s disease (AD): AD is clinically characterized by progressive memory loss and cognitive impairment. From a pathological point of view, the main features of AD are the deposition of amyloid plaques (composed of amyloid-beta, Aβ) and neurofibrillary tangles containing hyperphosphorylated Tau in the brain, accompanied by neuronal and synaptic loss, neuroinflammation and brain atrophy (Jellinger, 2022). Regardless of these common traits, growing evidence shows increased heterogeneity in the brain of AD patients considering both clinical manifestations and pathological features. Mounting evidence points to the variable conformations that misfolded Aβ can acquire (referred to as “Aβ strains”) as the source of this pathological and clinical variability. The existence of Aβ strains is relevant as they may also predict prognosis and responses to treatments. The concept of Aβ strains is analogous to that coined for infectious prion strains, which are further defined below (Jellinger, 2022).