Yeah, that sure seems to have come out of nowhere. Over lunch I did a bit of news reading to see if anything came up. This is all I get from the past few days:

• Fructose might be the cause of Alzheimer's (https://www.sciencealert.com/group-of-scientists-propose-a-new-driver-of-alzheimers-disease-fructose)
• Viruses (and maybe bacteria) might be the cause of Alzheimer's, and the article mentions lecanemab and how it's not that effective (https://www.theguardian.com/society/2023/feb/19/could-alzheimers-be-caused-by-an-infection)
• Another drug approach for dealing with amyloid plaque and its precursors (as I understand it), and it also mentions lecanemab in less-than-glowing terms (https://scitechdaily.com/groundbreaking-new-treatment-developed-for-alzheimers-disease/)

Maybe I missed something, but none of this seems that new. My understanding of the field is that we are still a long way away from a real knowledge of the cause and progress of the disease at a neurological level, and it seems to me that new hypotheses come up often.

So maybe the news is something to do with their 1H23 results.

(Disc: held in RL)

Following up on my last straw, it seems that the market didn't like the news from the lecanemab researchers. Here's an article by the same author in the Guardian (https://www.theguardian.com/society/2022/nov/30/drug-slows-cognitive-decline-in-alzheimers-patients-study-reveals) about the new data. As expected, the drug led to a 27% reduction in the reduction of cognition (ie. cognitive decline was slowed by the drug), but there were some safety issues.

The Guardian article doesn't go into them in detail, but reading the original article in the New England Journal of Medicine (paywalled, although you can get to a free short summary on the link without paid access) it looks like the authors' main concern is Amyloid-related Imaging Abnormalities (ARIA). I'm not qualified to comment authoritatively on the medical side of things, but from what I understand these ARIA are related to edema (ARIA-E) and haemorrhages (ARIA-H), which sound pretty bad, although they say that none of the deaths in the trial occurred with ARIA. At any rate, they seem to imply that these events weren't extremely serious, saying that the ARIA-E in particular were mostly mild to moderate (although they didn't give a definition of what "mild" or "moderate" is).

They also report a large number of patients getting infusion-related reactions, although again they said that these were mostly mild to moderate, and if the patients took a preventative medication then that helped them avoid reactions.

I guess a key metric for Cogstate is the "number of adverse events leading to discontinuation of the trial agent", which was 62 (6.9%) in the lecanemab group and only 26 (2.9%) in the placebo group. If the patient doesn't keep taking the medicine, then maybe they won't keep taking Cogstate's tests. But I don't know how to interpret those numbers in the context of other drugs (are they anything to worry about?), so I'll leave it to someone else.

So my takeaway on lecanemab: it's a drug that has the first real clinical effect on Alzeihmer's, but it's a small effect and patients are at an elevated risk of some serious side-effects, although in the trial so far no one has died from it. Hopefully we'll get better data on it in the next year or so, and hopefully^2 we'll get better iterations of the drug in future.

Takeaway for Cogstate: the trial could make FDA approval of lecanemab more difficult and so it could be a short/medium-term negative, but my longer-term thesis (that Cogstate are going to be involved in more and more clinical trials, and that there will be an effective Alzheimer's drug that clinicians can use Cogstate/'s test for monitoring) is intact and even strengthened.

(Disc: held)

More news to add to that from @GazD and @Chagsy This one's from The Guardian, talking about lecanemab specifically. It's a pretty good summary as it gives some context for the development of the drug and its shortcomings. The point is that even though this drug may not be great at treating Alzheimer’s, it's an indicator that there actually are pathways to treat the disease, which have been lacking up to now. So the reason researchers are so excited about lecanemab is that this could be the start of a process to find some really good treatments. The article ends with:

``And this is what the field needs, says [one of the scientists]: more funding, more approaches, more trials''.

This all sounds pretty good for Cogstate.

At any rate, the article says the lecanemab researchers will give an update on their trials today (San Francisco time), so we should get a better sense of things soon.

(Disc: held)