中国神经再生研究(英文版) ›› 2023, Vol. 18 ›› Issue (3): 529-530.doi: 10.4103/1673-5374.346476

• 观点:退行性病与再生 • 上一篇    下一篇

核氧还蛋白样2代谢信号会损害其对神经退行性疾病的潜在贡献

  

  • 出版日期:2023-03-15 发布日期:2022-08-26

Nucleoredoxin-like 2 metabolic signaling impairs its potential contribution to neurodegenerative diseases

Mariangela Corsi, Céline Jaillard, Thierry Léveillard*   

  1. Sorbonne Université, INSERM, CNRS, Institut de la Vision, Paris, France
  • Online:2023-03-15 Published:2022-08-26
  • Contact: Thierry Léveillard, PhD, thierry.leveillard@inserm.fr.
  • Supported by:
    This work was funded by the Agence Nationale pour la Recherche, Fondation Vaincre Alzheimer and Sorbonne Université.

摘要: https://orcid.org/0000-0001-5692-8770 (Thierry Léveillard)

Abstract: Alzheimer’s disease (AD) threatens the foundations of humanity and our society. AD is a neurological disorder primarily affecting the elderly through memory disorders, cognitive decline, and loss of autonomy. The dramatic consequences of this late-onset disease were illustrated sensitively in Michael Haneke’s masterpiece, Amour. Researchers and governments have invested colossal efforts to develop a treatment for this terrible disease. Currently and in the past decade the amyloid cascade has dominated the therapeutic research on AD, but the absence of benefit for patients treated with drugs that reduce brain amyloid deposit questions the role of β-amyloid as a causative agent (Herrup, 2021). The recent approval of aducanumab by the United States Food and Drug Administration, a drug that targets β-amyloid, is at the center of a scandal among clinicians and researchers, as it does not provide therapeutic benefits to patients and is listed among the breakdowns of the year 2021 by Science magazine (Voosen et al., 2021). The lack of progress in curing AD and recent therapeutic failures calls for further exploratory research.