EPISODE · May 19, 2026 · 19 MIN
997-低血糖与磷酸化Tau协同诱导神经元程序性坏死
from 聊聊Sci
这项研究揭示了大脑葡萄糖代谢不足与病理性Tau蛋白（p-Tau）协同诱发神经元死亡的分子机制。研究发现，在低血糖环境下，积累的p-Tau会充当分子支架招募RIPK1激酶，同时代谢压力导致保护性的检查点蛋白A20流失。这种双重作用激活了非凋亡性的程序性坏死（necroptosis）路径，最终导致脑萎缩和认知功能退化。实验证明，通过补充乙酰左旋肉碱（ALCAR）恢复A20水平，或干预p-Tau与RIPK1的结合，可以显著减轻小鼠模型中的神经退行性病变。该成果为理解阿尔茨海默病等疾病中代谢异常如何驱动神经元丢失提供了关键的机械性见解。References:Chen X, Li S, Neubauer A, et al. Glucose hypometabolism and hyperphosphorylated Tau synergistically drive neuronal necroptosis[J]. Neuron, 2026.前往小宇宙评论区与主播互动
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997-低血糖与磷酸化Tau协同诱导神经元程序性坏死
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