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.

人們很容易對(duì)宣稱(chēng)能減緩阿爾茨海默病(最常見(jiàn)的癡呆癥)進(jìn)展的藥物的公告持懷疑態(tài)度。然而，Lecanemab可能是真正的“解藥”。它的“制造商”東京的衛(wèi)材公司和馬薩諸塞州劍橋的渤健公司進(jìn)行的一項(xiàng)臨床試驗(yàn)的結(jié)果剛剛在《New England Journal of Medicine》上發(fā)表。在18個(gè)月后，它將癥狀的進(jìn)展速度減緩了四分之一。

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.

這項(xiàng)試驗(yàn)有1795名參與者參與，最重要的是，他們都處于疾病的早期階段。一半人接受了藥物治療。其他的則是使用安慰劑。這說(shuō)明了兩件事。一個(gè)是緩慢但可評(píng)估的進(jìn)展。另一個(gè)是對(duì)阿爾茨海默癥的一種解釋叫做淀粉樣蛋白假說(shuō)似乎是正確的。

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 -淀粉樣蛋白是一種沉積在阿爾茨海默病患者大腦中的蛋白質(zhì)斑塊。它和另一種蛋白質(zhì)tau都是這種疾病的癥狀。但究竟是其中之一還是兩者都是導(dǎo)致這種現(xiàn)象的根本原因，人們一直爭(zhēng)論不休。lecanemab的成功表明，β -淀粉樣蛋白確實(shí)直接引發(fā)了與癡呆相關(guān)的問(wèn)題。lecanemab是一種抗體，它可以附著在β -淀粉樣蛋白上，然后吸引免疫系統(tǒng)細(xì)胞將其清除掉(在接受藥物治療的患者身上確實(shí)做到了這一點(diǎn))。

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.

這只是小小的一步。一些專(zhuān)家質(zhì)疑用于顯示癥狀改善的測(cè)試是否具有臨床意義。此外，lecanemab在許多參與者身上引發(fā)了嚴(yán)重的副作用——尤其是大腦腫脹和出血。而且，這么早診斷出癡呆是很難的。β -淀粉樣蛋白可以通過(guò)正電子發(fā)射斷層掃描來(lái)檢測(cè)，但這需要昂貴的設(shè)備?；蛘呖梢蕴崛∧X脊液樣本，這是不愉快的，而且不容易變成常規(guī)篩查程序。不過(guò)，這是一個(gè)原理證明?，F(xiàn)在，抗體方法已經(jīng)被證明有效，后續(xù)可以使用其他類(lèi)似的抗體。希望很快有更多的好消息。