中国神经再生研究(英文版) ›› 2026, Vol. 21 ›› Issue (8): 3515-3516.doi: 10.4103/NRR.NRR-D-25-00464

• 观点:退行性病与再生 • 上一篇    下一篇

基于抑制双亮氨酸拉链激酶急性轴突棕榈酰化的新型神经保护策略

  

  • 出版日期:2026-08-18 发布日期:2026-04-25

Novel neuroprotective strategy based on inhibition of acute, axonal palmitoylation of DLK

Azita Minaei, Xiaotian Zhang, Gareth M. Thomas*   

  1. Center for Neural Development and Repair, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, USA (Minaei A, Zhang X, Thomas GM) 
    Department of Neural Sciences, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, USA (Thomas GM)
  • Online:2026-08-18 Published:2026-04-25
  • Contact: Gareth M. Thomas, PhD, gareth.thomas@temple.edu.
  • Supported by:
    This work was supported by NIH (R01 NS094402 and R21 EY029386) Shriners Children’s (#85190 PHI and #87400 PHI) and by BrightFocus Foundation (G2019267) (to GMT).

摘要: https://orcid.org/0000-0003-3183-8431 (Gareth M. Thomas)
 

Abstract: The field of neurodegeneration research has long been focused on finding therapeutic strategies to effectively decrease or halt neuronal loss while minimizing side effects. A recent study titled “Inhibiting acute, axonal DLK palmitoylation is neuroprotective and avoids deleterious effects of cell-wide DLK inhibition”(Zhang et al., 2025), describes an innovative approach to achieve this goal. The authors target a specific posttranslational modification of dual leucine-zipper kinase (DLK), palmitoylation, to selectively inhibit DLK-dependent pro-degenerative signaling and protect neurons, thereby revealing a new way to intervene and block neurodegeneration. This Perspective aims to explore the significance of these findings and propose directions for future research.