GLP-1 agonist didn't stop progression of AD in patients who were already on the disease course. I haven't read the protocol (if they enrolled in the EU it's out there somewhere), but I'd bet that the inclusion criteria included something about amyloid positivity, either in the blood, CSF, or from PET imaging.
What does that mean? It means that GLP-1 agonists may still prevent AD from being as likely to occur through indirect mechansims (i.e., obesity is tied to AD, less likelihood of developing AD if healthy weight), but probably can't slow it down once it's started, e.g., amyloid is laid out and tau is starting to pile up along that trailblaze from the amyloid.
Congrats, you've read an actual intelligent comment from someone with relevant knowledge and experience.
I mean sure, the average layperson is gonna fuck it up. But what about professionals, e.g., a PhD scientist?
I use LLM-based models for lit searches (typically, these are dedicated tools for lit searches, but I have tried it on ChatGPT). I don't use the summaries, but I do use the lists of papers it comes up with and generally go through them in whatever ranking it spits out.
Works pretty well, saves a ton of time in *starting* lit searches. Still have to do the reading. The AI sucks at interpreting papers, wouldn't ever trust it as it stands now.
Hi, scientist overseeing clinical trials involving AD! I wouldn't say the jury is still out on the importance of amyloid as a biomarker in assessing AD progression and response to treatment. Patients using the now FDA-approved anti-amyloids had statistically significant reduction in rate of decline as compared to placebo, assessed by cognitive tests. They also had reduction in amyloid load, as assessed via amyloid PET.
The previous 20 years may have failed. That doesn't mean today's drug pipeline is also going to fail.
"Open Channel D..." -- Napoleon Solo, The Man From U.N.C.L.E.