Neural Regeneration Research ›› 2026, Vol. 21 ›› Issue (7): 2824-2825.doi: 10.4103/NRR.NRR-D-25-00557

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Pathogenic landscape shaped by cerebral amyloid oligomers

Yujing Huang# , Mengze Xu# , Zhen Yuan* , Pu Chun Ke*   

  1. Faculty of Health Sciences, University of Macau, Macao Special Administrative Region, China (Huang Y, Yuan Z) Department of Biology, Faculty of Arts and Sciences, Beijing Normal University, Zhuhai, Guangdong Province, China (Xu M) Center for Cognitive and Brain Sciences, University of Macau, Macao Special Administrative Region, China (Xu M, Yuan Z) Drug Delivery, Disposition and Dynamics, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, VIC, Australia (Ke PC)
  • Online:2026-07-15 Published:2025-10-20
  • Contact: Zhen Yuan, PhD, zhenyuan@um.edu.mo; Pu Chun Ke, PhD, pu-chun.ke@monash.edu.
  • Supported by:
    We acknowledge Professors Colin Masters and Scott Ayton from Florey Institute, The University of Melbourne, Australia for discussions. This work was supported by the National Key Research and Development Program of China (2021YFA1200900 and 2022YFC2409700) and the Distinguished Visiting Scholar Program with the University of Macau (to PCK).

Abstract: Amyloid oligomers, a brief history: Amyloid d i s e a s e s e n c o m p a s s a r a n g e o f h u m a n neurological, systemic, and metabolic disorders, characterized by the common feature of amyloid fibril and plaque deposition, either intracellularly or extracellularly. Among them, Alzheimer’s disease (AD)—manifested by memory loss and cognitive decline—and Parkinson’s disease (PD)— underlined by impaired dopamine release and motor dysfunction—are the two most prevalent forms of neurodegenerative conditions that have rapidly become global epidemics. Type 2 diabetes, conversely, is a prevalent metabolic disorder underpinned by pancreatic beta cell loss, elicited primarily by the aggregation and toxicity of human islet amyloid peptide.