Our microglia janitor cells become hyper-activated, releasing chemicals that cause inflammation and cellular damage. 我们的小神经胶质细胞变得过度活跃，释放出导致炎症和细胞损伤的化学物质。

　　We think they might actually start clearing away the synapses themselves. 我们认为这可能会清除突触本身。

　　A crucial neural transport protein called "tau" becomes hyperphosphorylated and twists itself into something called "tangles," 一种叫做tau蛋白的神经转运蛋白变得过度磷酸化,并转化成叫做神经纤维缠结的物质，

　　which choke off the neurons from the inside. 从内部阻塞了神经元。

　　By mid-stage Alzheimer's, we have massive inflammation and tangles and all-out war at the synapse and cell death. 在老年痴呆症的中期，我们会面临大量的炎症和神经纤维缠结、突触处的全面战争以及细胞的凋亡。

　　So if you were a scientist trying to cure this disease, at what point would you ideally want to intervene? 如果你是一位想要治愈该病的科学家，最佳介入时机是什么时候呢？

　　Many scientists are betting big on the simplest solution: keep amyloid plaques from reaching that tipping point, 许多科学家赌在了最简单的解决方法上：避免淀粉样斑块达到临界点，

　　which means that drug discovery is largely focused on developing a compound that will prevent, eliminate, or reduce amyloid plaque accumulation. 也就意味着药物研发很大程度上聚焦于研发一种可以预防、消除或是减少淀粉样斑块积累的化合物。

　　And so the cure for Alzheimer's will likely be a preventative medicine. 所以老年痴呆症的治疗方法很有可能是一种预防性的药物。

　　We're going to have to take this pill before we reach that tipping point, 我们需要在临界点到达之前，

　　before the cascade is triggered, before we start leaving our keys in the refrigerator. 在连锁反应产生之前，在我们把钥匙落在冰箱前服用这种药物。

　　We think this is why, to date, these kinds of drugs have failed in clinical trials 我们认为这也是迄今为止这类药物在临床试验上失败的原因，

　　not because the science wasn't sound, but because the people in these trials were already symptomatic. 并不是因为科学技术不够可靠，而是因为在临床试验的人们都已是老年痴呆的患者。

　　It was too late. Think of amyloid plaques as a lit match. 这就为时已晚。试想淀粉样斑块是已经点燃的火柴。

　　At the tipping point, the match sets fire to the forest. 在临界点后，火柴的火引燃了整片森林。

　　Once the forest is ablaze, it doesn't do any good to blow out the match. 一旦森林起火，吹灭火柴早已于事无补。

　　You have to blow out the match before the forest catches fire. 你需要在火柴引燃森林前就把火柴熄灭。