this post was submitted on 07 Jul 2023
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Japanese drugmaker Eisai and US-based Biogen have been working together on advancing research in the space of Alzheimer’s for nearly a decade. Finally, the FDA, granted the fruits of that labor, Leqembi, its blessing for intravenous use. This marks the first approved treatment that can slow the progression of Alzheimer’s.

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[–] [email protected] 78 points 1 year ago* (last edited 1 year ago) (2 children)

For those interested. This is similar to Aduhelm in that it is an amyloid binding drug. Amyloids proteins have long been thought to be central to Alzheimer's disease since it was first described by Dr. Alois Alzheimer in 1906, where during his autopsy of a 50-year who died while suffering memory loss, disorientation, and other classical symptoms of the disease noticed "senile plaque" had accumulated on the brain which is usually found in much older patients. In the 1980s chemical analysis of the plaque indicated that it was made of beta-amyloids and from there we've been attempting to target that in order to prevent Alzheimer's disease.

The statement that the drug "will" slow Alzheimer's is editorial so to say. After their third phase trail, the results were sobering.

27% decrease in the rate of progression for patients treated with Leqembi, compared to those receiving a placebo.

Which 27% is still 27%. But this drug is looking to go for a price of $23,000 to $27,000 per year (drug cost alone, infusion and doctor's office visits may shoot this price upward towards $90,000/year). Strangely the article says:

Current rules mean that it’s unlikely to be covered by Medicare.

Which there was Senate hearing where the exact opposite was indicated. Medicaid will likely have the 20% co-pay for patients. That said, for the United States, this drug will be outside of the reach of many not 65 or older.

Additionally, we're still at the nexus of this topic and not knowing full well where to go for the treatment in Alzheimer's. Many competing ideas of the full scope of Alzheimer's disease still exist from tau tangles to neuron degeneration. It's indisputable that beta-amyloids do have a part in Alzheimer's the question remains as to how large a role it plays in mental decline and the low positive outcomes of beta-amyloids has served as fuel for discussion of other ideas. That said, penicillin failed twice in clinical trials, but today nobody would question antibiotic theory, so take the failures with a grain of salt perhaps? But this all does indeed go to show, this area of research is dizzily complex and fluid to say the least.

As for the "first" distinction and that Aduhelm has been FDA approved since 2021. Leqembi is the FIRST to receive the full FDA approval. Aduhelm still operates under the accelerated approval and is still pending a full review. Much like how we had COVID vaccines approved under the accelerated program first and then in 2022 the FDA gave many of them full approval.

It's good this drug has received the first full approval for the treatment of beta-amyloids. But suffice to say, based on the approval material, we still have yet a LONG way to go in Alzheimer's research.

[–] [email protected] 27 points 1 year ago

This is the first time I’ve opened a post on Lemmy and seen such a valuable response. Thanks for being here and taking the time to post this. Super interesting and informative stuff.

My ex wife’s dad is in the middle stages of early onset dementia (he’s in his mid-60’s) and I’m thinking it’s a bit too late for this to be helpful. But seeing this progress gives me hope for my ex-wife and her brother who both have very high risk of dementia (grandma, their dad, and their uncle all suffer(ed) from it, dad and uncle are both in similar stages with dad a couple years behind uncle… really sad shit).

I really hope we get this figured out in the next 20 years.

[–] [email protected] 3 points 1 year ago

We are starting to see the first drugs on the market that utilize the amyloid beta pathway in some fashion because research in the 90's and 2000's were absolutely convinced that this pathway was the lynchpin to the disease. My understanding of the disease (I studied biotech but not Alzheimer's specifically) is that amyloid beta plaques are more of a side effect of whatever is really going on than the main show. And unfortunately the mechanism of dementia in general is not really well understood, Alzheimer's included.

These sobering results are not really that surprising because treating the amyloid beta plaques after they have formed is sort of like trying to prevent spoiled meat by removing the maggots that have accumulated on it.