<i>Trans ε</i> viniferin decreases amyloid deposits and inflammation in a mouse transgenic Alzheimer model

As Alzheimer’s disease (AD) induces several cellular and molecular damages, it could be interesting to use multi-target molecules for therapeutics. We previously published that trans ε-viniferin induced the disaggregation of Aβ42 peptide and inhibited the inflammatory response in primary cellular model of AD. Here, effects of this stilbenoid were evaluated in transgenic APPswePS1dE9 mice. We report that trans ε-viniferin could go through the blood brain barrier, reduces size and density of amyloid deposits and decreases reactivity of astrocytes and microglia, after a weekly intraperitoneal injection at 10 mg/kg from 3 to 6 months of age.阿尔茨海默病（Alzheimer’s disease, AD）可引发多种细胞与分子层面的损伤，因此采用多靶点分子进行治疗具备重要研究价值。我们此前已发表研究表明，反式ε-葡萄素（trans ε-viniferin）可诱导Aβ42肽解聚，并在阿尔茨海默病原代细胞模型中抑制炎症应答。本研究针对该芪类化合物（stilbenoid）在转基因APPswePS1dE9小鼠中的药效展开评估。结果显示，于小鼠3月龄至6月龄期间，每周以10 mg/kg的剂量进行腹腔注射后，反式ε-葡萄素可穿过血脑屏障（blood brain barrier），减小淀粉样蛋白沉积的大小与密度，并降低星形胶质细胞与小胶质细胞的反应性。