每天一篇经济学人 | A drug for Alzheimer's diseas

It is easy to be cynical about announcements of drugs that claim to slow the progress of Alzheimer’s disease, the most common form of dementia. Lecanemab, however, may be the real deal. Results of a clinical trial, conducted by its makers, Eisai, of Tokyo, and Biogen, of Cambridge, Massachusetts, have just been announced in the New England Journal of Medicine. After 18 months, it had slowed the progress of symptoms by a quarter.

人们很容易对宣称能减缓阿尔茨海默病(最常见的痴呆症)进展的药物的公告持怀疑态度。然而，Lecanemab可能是真正的“解药”。它的“制造商”东京的卫材公司和马萨诸塞州剑桥的渤健公司进行的一项临床试验的结果刚刚在《New England Journal of Medicine》上发表。在18个月后，它将症状的进展速度减缓了四分之一。

The trial involved 1,795 participants who were, crucially, in the early stages of the illness. Half received the drug. The others, a placebo. It showed two things. One was that modest but measurable slowing of progression. The other was that an explanation of Alzheimer’s called the amyloid hypothesis seems correct.

这项试验有1795名参与者参与，最重要的是，他们都处于疾病的早期阶段。一半人接受了药物治疗。其他的则是使用安慰剂。这说明了两件事。一个是缓慢但可评估的进展。另一个是对阿尔茨海默症的一种解释叫做淀粉样蛋白假说似乎是正确的。

Beta-amyloid is a protein which accumulates in plaques in the brains of those with Alzheimer’s. It, and a second protein, tau, are established signs of the illness. But whether either or both is a root cause of it has been much debated. The success of lecanemab, an antibody that attaches itself to beta-amyloid and then attracts immune-system cells which clear the protein away (and measurably did so in those receiving the drug), suggests beta-amyloid does indeed directly create problems associated with dementia.

β -淀粉样蛋白是一种沉积在阿尔茨海默病患者大脑中的蛋白质斑块。它和另一种蛋白质tau都是这种疾病的症状。但究竟是其中之一还是两者都是导致这种现象的根本原因，人们一直争论不休。lecanemab的成功表明，β -淀粉样蛋白确实直接引发了与痴呆相关的问题。lecanemab是一种抗体，它可以附着在β -淀粉样蛋白上，然后吸引免疫系统细胞将其清除掉(在接受药物治疗的患者身上确实做到了这一点)。

This is a small first step. Some experts question whether the test used to show an improvement in symptoms is clinically meaningful. And lecanemab induced nasty side-effects—notably swelling and bleeding of the brain—in a number of participants. Also, diagnosing dementia this early is hard. Beta-amyloid can be detected by positron-emission tomography, but that requires a piece of expensive equipment. Or a sample of cerebrospinal fluid can be taken, which is unpleasant, and not something that could easily be turned into a routine screening programme. It is, however, a proof of principle. Now that the antibody approach has been shown to work, it can be followed up with other, similar, antibodies. Hope for more good news soon.

这只是小小的一步。一些专家质疑用于显示症状改善的测试是否具有临床意义。此外，lecanemab在许多参与者身上引发了严重的副作用——尤其是大脑肿胀和出血。而且，这么早诊断出痴呆是很难的。β -淀粉样蛋白可以通过正电子发射断层扫描来检测，但这需要昂贵的设备。或者可以提取脑脊液样本，这是不愉快的，而且不容易变成常规筛查程序。不过，这是一个原理证明。现在，抗体方法已经被证明有效，后续可以使用其他类似的抗体。希望很快有更多的好消息。