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!
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 …
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
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?
