在多發性硬化症的病理進程中，少突膠質細胞的成熟與髓鞘重建是一項關鍵挑戰。本集深入探討UBE3A的上調表現如何影響細胞命運決定與髓鞘形成，連結小鼠模型與人類資料，試圖釐清UBE3A是否為限制神經修復的核心節點，並探討其作為治療靶點的可能性。
Myelin repair is a cornerstone challenge in MS.This deep-dive explores how UBE3A upregulation disrupts oligodendrocyte lineage progression and impairs remyelination. Drawing from both mouse models and human studies, we examine whether UBE3A represents a central molecular brake—and a viable therapeutic target—for neuroregeneration.
-
📝
https://doi.org/10.1038/s41467-025-62053-w
-
TBAL 台灣活性脂質股份有限公司
官網 https://www.t-bal.com/
粉絲臉書團 https://www.facebook.com/TBAL2017
YOUTUBE https://www.youtube.com/@Taiwan-BioActive-Lipid
The recipient's phone：+886-4-2247-6758
Customer service email：t-bal_2@t-bal.com.tw