Lecanemab and the new potential of anti-abeta therapies for Alzheimer's
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- čas přidán 26. 07. 2024
- This topic is particularly near and dear to my heart as I worked in the industry generating Alzheimer's drugs for the past year. Lecanemab (Lacembi) is generating headlines all over the place this year so I wanted to chime in and talk about how it works and how it fits with other current treatments.
As always, feel free to check my sources and add anything I might have missed in the comment :)
Nicely done summary of a very complex topic. I've been participating in a number of Alzheimer's studies (in honor of my father and grandmother who dealt with it). I applied for a clinical study for lecanemab (AHEAD-3/4) which is looking at the impact of this drug on individuals who have not yet reached the MCI phase - essentially seeing if removal of the amyloids at an earlier stage will prevent the patient even getting into the downward Alzheimer's impact. Unfortunately, although I passed all the other criteria (no ARIA, no APOE-4, etc.) when I had a PET scan the result was that I had no amyloids in my brain, hence there was nothing to remove. I was disappointed but remain committed to participating in various Alzheimer's testing programs - even if it's just as a control. I have shared all the details in a blog which I maintain. Thanks again for a great summary!
I followed the controverial development of Lecanemab and Aducanumab but I never really bothered to look too much into the clinical trials (It's quite unrelated to what I work on). This was a very nicely put summary, so thank you for that!
excelent video ! can you do more of these explaining the mecanism of the treatments ? really good job of simplification
It’s great to see a woman discuss science on International Women’s Day
I was approved for Leqembi . 2 days before my IV was scheduled, I found about ARIA by myself. I immediately refused the drug.
I had a brain bleed in 2007. My neurologist is a do nothing …
How about using CT to get through the brain blood barrier while administrating the drug
I can't help but wonder if the increased risk of ARIA isn't because the plagues are more stubborn to remove than is desirable. Beyond the potential inflammation from the immune response, I wonder if the amyloid plagues are reforming/recombining whilst being removed from the brain/handled by the immune system. I haven't read any of the studies but I'd be super curious if there were any abnormalities in treated patients' lymphatic fluids at different periods of time after their treatment(s).
Also a video covering Tau related treatments would be something I'd love to see.
A Tau video will be upcoming! There are certainly connections to lymphatic function, especially in patients with APOE4 which tend to have impaired drainage, but I think the link has yet to be fully illuminated. But I imagine treating earlier would lead to less "stubborn" plaques
@@TheLabMouse I'm looking forward to it then and I also agree that it would seem like earlier treatment would lead to less headaches, pun intended.
I have MCI and abnormal CSF for Alzheimer’s with a normal level of TAU-P. I saw a new article that suggests with low TAU that Luqembi is much more effective. Do you have any insight
Thanks for the comment! I imagine the reason why low tau is correlated to better outcomes is because low tau means that you are very early in the disease and Lecanemab is better suited for early stages/prevention.
Is there the possibility that Lecanemab works on something other than just amyloid? Or is the reduction of amyloid plaques clearly how it benefits the patient?
I haven't heard anything about off-target binding, but we can never rule it out! The idea is that any and all effects are due to amyloid binding.
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