Lecanemab Graduates

We wrote in January that lecanemab (marketed as Leqembi) had been approved by the FDA to treat Alzheimer's disease.  This was the consequence of a fast-track approval based on the phase 2 trial, so it was a kind of provisional approval.  Normally, approval is based on the phase 3 trial, and that wasn't complete yet.  And after the phase 3 trial is done, an advisory panel normally reviews the trial data and recommends approval.  In this case, that's the Peripheral and Central Nervous System Drugs Advisory Committee (PCNS).  

You will recall that when aducanumab (now Aduhelm) hit this stage, several members of the advisory panel disagreed that the treatment should be approved.  When the FDA approved it anyway, several members of the panel resigned. 

Things are calmer for lecanemab.  The PCNS has just voted unanimously to recommend approval of the treatment.  I understand the naysayers from the aducanumab days are no longer on the panel, but we also know more about how these monoclonal antibody treatments work for Alzheimer's disease.  Although lecanemab was provisionally approved in January based on the phase 2 trial data, what this vote does is make the approval more conventional ... and more convincing.  No shortcuts.  The phase 3 trial is done, and the PCNS has now reviewed all of the data.  They are unanimously comfortable in recommending that the FDA approve the treatment for use.

Lecanemab does not cure Alzheimer's disease, it just slows its progress.  This appears to be because it is treating symptoms, not the disease itself.  It appears that amyloid plaques are interfering with how the brain functions and may be killing brain cells.  Clearly, getting rid of them helps with memory and cognition, at least for some people.  But why are the plaques forming in the first place, and how do you stop that?  Do the plaques actually form for a good reason, perhaps to protect the brain from bacteria and viruses?  The more we learn, the more questions we find ourselves asking.