中国神经再生研究(英文版) ›› 2024, Vol. 19 ›› Issue (9): 1871-1872.doi: 10.4103/1673-5374.390983

• 观点:退行性病与再生 • 上一篇    下一篇

高毒性的β淀粉样蛋白引发更多的β淀粉状蛋白

  

  • 出版日期:2024-09-15 发布日期:2024-01-25

Highly toxic Aβ begets more Aβ

Merc M. Kemeh, Noel D. Lazo*   

  1. Gustaf H. Carlson School of Chemistry and Biochemistry, Clark University, Worcester, MA, USA
  • Online:2024-09-15 Published:2024-01-25
  • Contact: Noel D. Lazo, PhD, NLazo@clarku.edu.
  • Supported by:
    This work was supported by the National Institutes of Health through grant R15AG055043 to NDL and also by the Lise Ann and Leo Beaver’s endowment to Clark University. 

摘要: https://orcid.org/0000-0003-1769-7572 (Noel D. Lazo)

Abstract: Alzheimer’s disease (AD) is the most common form of dementia-the 7th leading cause of death worldwide. At the tissue level, AD is characterized by the presence of extracellular amyloid plaques that are comprised primarily of the amyloid-β peptide (Aβ), and by intraneuronal neurofibrillary tangles composed of tau. Molecular genetics of early-onset AD and longitudinal brain-imaging studies of late-onset AD indicate that extracellular Aβ deposition, in general, precedes neurofibrillary tangle formation in neurons (Hampel et al., 2021; Young-Pearse et al., 2023).