Lecanemab approved!

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Re: Lecanemab approved!

Post by floramaria »

broiler_x wrote: Fri Jan 06, 2023 6:36 pm I really hope I'm wrong - I hope it works!! But, I have a 20+ year career in antibody therapeutics, including 2 different projects for antibodies against ABeta (beta amyloid), and for one I was the leader of the project. So I know this field really well. Let's not forget the scandal from a few months ago that exposed fraud in the amyloid theory with doctored data from a seminal paper.
Thanks for adding your insights and experience to the discussion.
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Re: Lecanemab approved!

Post by J11 »

broiler_x, thank you for replying.

I really do not understand this in terms of being right or wrong. In an earlier post on the Aducan thread, I think I got closest to the truth when I described it in terms of Smith's invisible hand idea -- as long as everyone pulls on that tug of war rope for what they believe then you will reach closest to an optimal outcome that reflects all viewpoints. It is only when you don't have that full commitment that the outcome isn't the best. This seems to perhaps have happened with the Lecanemab result. After the CMS discussions I became resigned to the idea that we would just roll forward in time until Clarity reported and then some time later the FDA would decide on the PDUFA date. Yet, in the documents today the FDA indicated that they were entirely unaware of the results of Clarity and expect to receive these results by March 2023. Hmm, should we sent them the NEJM article from 3 months ago? If we had been pulling with all our might on that rope then perhaps we could have moved up the PDUFA to August and then they could have decided for full approval when Clarity was officially over.

Of course, the problem is that out in the real world it really does not work like that. People become psychologically committed to some position and then to maintain cognitive coherence they become unwilling to concede ground. Life becomes a real grudge match. For some beta amyloid mabs in AD probably has become such a grudge match. Not for me, though. I see it as everyone putting forth their own perspectives and then through some sort of magical process the best result emerges.

In terms of my understanding of AD and amyloid, I see it as amyloid as the central spark of AD neuropathology. This is exactly why pharma has become so dominant in their focus of amyloid. Pharma wants to be as far upstream as possible. Amyloid is the most upstream there is. I suspect that those pharma companies that have been in business through the centuries realize how strategically important it is to claim the high ground. Once they are well entrenched up river, they can then shut off the water supply to everyone down stream and there will then be no benefit with the treatments that the others offer. The other treatments might now show better efficacy, yet that is merely because the mabs are still treating once the disease process is well established.

We already know with Aducan that dementia will never manifest if the antibody is given early enough. This is the result observed in the reverse translation research. Aducan is a naturally occurring, effective, safe and inexpensive treatment when dosed in the pre-MCI setting. Aducan did not demonstrate these features when it was mega dosed in a clinical dementia phase of the illness. I largely think that we have become stuck in a false narrative that the clinical trial process is the only way to move helpful products to market. With what we know now, we could go back in time 15 years and tell the FDA to simply approve Aducan as a low dose preventive for AD and this would have worked out so much better for the patients. Yet, these patients then progressed over all of these years and now they are being treated with upwards a gram of Lecanemab and this can cause side effects.
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Re: Lecanemab approved!

Post by J11 »

Flora please!

I am really starting to believe in me. J11 is a somebody. It is very discouraging when the people mock J11.
It feels that I am starting to make a real contribution to the conversation.

"q without a u" might not be the pinnacle of my contribution, though it is at least something.
Three other scrabble "q without a u" words are qat, burqa and qabbalah. It will be very interesting to
see how people actually pronounce Leqembi. It might be one of those times where everyone has a nervous
laugh and pronounce Lehimhimbi into their handkerchiefs until it is all sorted out. One can only wonder
how many patients might not receive treatment because they are unable to pronounce the Abracadabra word.
I think as a fall back it would be best to stick with Lecanemab.
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Re: Lecanemab approved!

Post by J11 »

So my basic point of view is that amyloid truly is the pressure point that will lead to effective AD treatments. My perception is that there is also a covert lobbying effort by payors to distort and subvert the truth about amyloid. There are clearly corporate shills, and there are also somewhat more hidden other shills who have ulterior motives. At some point I think the FDA accumulated overwhelming evidence in favor of mabs and then entered the process as an amyloid ally. They must have realized that those tens of millions of clinical AD patients could be helped and the only moral thing to do was to join the team. That is possibly how we wound up with the recent congressional report investigating the partnership between the FDA and Biogen.

Lecanemab is the next generation mab and it is clearly a better product. I have only realized that Lecanemab has been priced below Aducanumab and this is a great price strategy to quietly sideline Aducanumab without having to officially delist it. People can simply follow the price signal and get a better product. Pivoting to Leca is a natural evolution in my support of anti-amyloid treatments. With an approved product we can now turbo charge the push forward as there is finally a funding source available which will allow more of the market potential to be realized. Not investing in Leca now has a clear financial cost.

With the doctored data, I see that more as a sleeper story that could be reinvigorated once the amyloid story was reaching the finish line. The idea that modern science can somehow be disproven by any single paper would only seem plausible by those outside of science. It was meant to cast doubt on the amyloid hypothesis on mainstream street and not so much in the academic labs. The actual clinical results from Clarity have now largely placed the amyloid hypothesis beyond reasonable disagreement. With that victory in hand, other aspects of mabs can be strengthened (e.g., safety).

Yes, we saw that with Aducan as well. If patients do not move to amyloid negative by the end of the 18 months of on core treatment, then they can rapidly decline. This was one of the more memorable results for me from Emerge/Engage high dose. The high dose patients that did not become amyloid negative had rapid decline; the amyloid negatives almost to a patient did not undergo this precipitous decline. Just looking at averages completely misses this result. One suspects that those who do enter rapid decline will be the ones who self-select out of the trial.

I went through this on the Aducan trial. There does seem to be ongoing benefit from mab treatment. This was seen with CDR-sb and the other measures. Once again though the clinical science is still somewhat weak. Clarity only used single selection using amyloid PET. Trailblazer used amyloid and tau PET selection. In a few months we will see how this might powerfully enhance the signal from that phase 3 trial.

I find this an interesting perspective that you think that Lecanemab will flop. Today I posted to the Aducan thread the CDR-sb percentile distributions from the phase 2 Leca trial by dosing arms. What I found of great interest is how such a great percentage of patients on high dose actually did quite well. About 75% of these patients were stable over 18 months. This insight was almost completely hidden when only thinking in terms of the 0.45 benefit.

What this suggests to me is that once patients are on Leca treatment most will be quite happy. Not that many of them will be decliners. Those that are might be encouraged to stop treatment. You then wind up with a great many happy patients. Those not on treatment in a waiting room non-treatment control group would then be seen to perform much worse. It would be a simple demonstration to doctors that treatment does help their patients; outside of the fairly artificial context of a clinical trial. Such a comparison would actually be at least somewhat an illusion because about 20% of the placebo actually improved and perhaps 40% of placebo were stable or better , though from the perspective of the treated patient who was stable or better this would not be observable. And as I have noted elsewhere this non-decliner/improver subset of placebo really should never have been considered as part of the AD population. The 10% of rapid decliners on treatment probably also should never have been considered either as they were too far into tau neuropathy.

So, basically my perception is that Lecanemab will not flop because so many typical Leca treated patients will actually be quite stable, not withstanding the seemingly smallish topline number. I will be very eager to see how these distributions worked out for the Clarity trial.

Of course, now that we have the first line of treatment with the mabs, there is no reason why we can't push for the second line. Combination treatment? Shutting down amyloid step one; shutting down tau step two. It is possible that we could see an approval this year for LMTM. That would be amazing! That is what the drug cocktail approach is all about. This combo perhaps could be roughly additive and we could then see large treatment effects. Once the force of neuropathology is removed, then all the downstream treatments would have a great chance to help patients further. Getting that foot in the door can make all the difference.

With other illnesses such as cancer, the entire foundational base of treatment (i.e., chemotherapy radiation, and surgery) are often so ineffective that it is not easy to build off them. However, when you can start with a reasonably effective treatment such as mabs, then you have the potential to move towards highly effective combinations. With a funded base treatment, there could be a financial motivation to build from this foundation.
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Re: Lecanemab approved!

Post by NF52 »

broiler_x wrote: Fri Jan 06, 2023 2:17 pm...there does appear to be a reduction in cognitive decline at the beginning of dosing. However, that benefit appears to go away after 6-9 months....


The data I'm referring to is Fig. 9 which shows the cognitive efficacy graphs....

And patients must start taking this years before showing any significant cognitive decline. And we won't even know if those patients will actually ever develop AD....
I applaud this effort. But I don't see this as actually doing much to help people I'm afraid.
Hi broiler_x,

You have many years of research in this field, and obviously care deeply about the effort, as noted in your last paragraph.

The figure you reference is from an early 2022 analysis of the PHASE 2 CORE 201 study of lecanamab at various doses against a placebo, in which the vast majority of ApoE4 carriers were removed from 10mg/kg of weight/biweekly dose after a decision by European regulators.

A total of 247 people received the final 10mg/kg biweekly dose in CORE 202.
898 were on that dose in CLARITY; providing more than 4x the sample size from which to analyze data.

CORE 202 had 93.7% of participants from N. America or Western Europe; the OLE of CORE 202 for some reason had 21.4% of people from Japan or Korea, representing a possible confounding factor in interpreting changes over. time.

Lecanemab in Early Alzheimer’s Disease was published in The New England Journal of Medicine on 11/29/2022 and is available with a free subscription that allows downloading of 2 articles per month. The article does not include OLE top-line results, which will be available later this year or early 2024.

In CLARITY, approximately 1/4 of participants self-identified as Hispanic, Asian or Black, following intensive efforts to recruit a population with racial/ethnic diversity
Lecanemab Arm : 76.3% White; 12.% Hispanic; 17.1% Asian; 2.3% Black.
Placebo Arm: 77.4% White; 12.3% Hispanic: 16.9% Asian; 2.7% Black

The study organizers sought to include comorbidities seen in typical AD populations, as seen in the screenshot from CTAD on 11/29::
Image 1-7-23 at 1.36 PM.jpeg
Lecanemab in Early Alzheimer’s Disease does provide some of the safety and efficacy data in CLARITY. The efficacy charts below show a positive trend line, which increases over time for some measures--and will be further studied for up to 36 months total from OLE.
Image 1-7-23 at 12.40 PM.jpeg
Image 1-7-23 at 12.39 PM.jpeg

I especially was impressed by the 37% less decline on functional skills meaningful to participants and families. The trend line seems to increase over time. [Alzheimer's Disease Cooperative Study-Activities of Daily Living Scale adapted for MCI: (ADCS-MCI-ADL), shown as CTAD]:
Image 1-7-23 at 1.43 PM.jpeg
In terms of rigor for design and safety, here's some info from the same NEJM article that suggests the placebo and lecanemab arms were well-balanced, and safety was monitored :
The randomization was stratified according to clinical subgroup (mild cognitive impairment due to Alzheimer’s disease or mild Alzheimer’s disease–related dementia..., the presence or absence of concomitant approved medication for symptoms of Alzheimer’s disease at baseline (e.g., acetylcholinesterase inhibitors, memantine, or both), apolipoprotein E (ApoE) ε4 carriers or noncarriers, and geographic region...The trial was conducted in accordance with International Council for Harmonisation guidelines and the ethical principles of the Declaration of Helsinki. The trial was approved by the institutional review board or independent ethics committee at each center, and all the participants provided written informed consent...An independent data and safety monitoring board consisting of experts in Alzheimer’s disease and statistics reviewed unblinded safety data during the trial. An independent medical monitoring team, whose members were unaware of the trial-group assignments, reviewed ARIA, infusion-related reactions, and hypersensitivity reactions. Clinical assessment raters were unaware of the safety assessments and the trial-group assignments.
I value your expertise and would welcome your views on the data of CLARITY efficacy.
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Re: Lecanemab approved!

Post by Julie G »

I wish this were cause for celebration. Lecanamab is covered in this retrospective: The Reason There's Been No Cure for Alzheimer's.
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Re: Lecanemab approved!

Post by circular »

J11 wrote: Fri Jan 06, 2023 4:17 pmAs it is now the million mile stare wasn't only how our demented relatives looked at us as the illness progressed, but also how we stared out to the community while we tried to cope with the AD in our life.
:( So well put J11, and hard not to take in with a wide open heart.
ApoE 3/4 > Thanks in advance for any responses made to my posts.
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Re: Lecanemab approved!

Post by broiler_x »

Julie G wrote: Sat Jan 07, 2023 12:06 pm I wish this were cause for celebration. Lecanamab is covered in this retrospective: The Reason There's Been No Cure for Alzheimer's.
Pretty brutal, but honest assessment. Thanks for sharing that. I think amyloid may have a role in disease, but not at the near exclusion of all other theories. I was a huge proponent of anti-amyloid therapeutics in the mid-2000's when the company that I worked for was developing an amyloid antibody. But there have been so many failures in the theory. For me, the final nail in the coffin was the BACE inhibitors. These block a protease that produces beta-amyloid from a precursor protein. They are tremendously effective at drastically reducing beta-amyloid burden. But, in clinical trials not only did they not reduce cognitive decline, it actually accelerated! So a drastic reduction in brain amyloid cause more decline. That was it for me.

Again, I like the excitement that this new antibody brings to the field. I just worry that if it does flop, or have significant side-effects, that it will sour further investment into AD research for years.
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Re: Lecanemab approved!

Post by J11 »

Broiler_x, I will take your comments line by line.

I think this is another poor decision by the FDA, but not as bad as for Aduhelm.

I do not think the FDA realistically had any other option then some variant of approval. It might have put a black box warning for tPA, or restriction on anti-coagulant use, though on the topline yea or nay for lecanemab I really do not see a way to nay. This will likely be verified as other health authorities decide on this. It is not easy to see them rejecting it. When the FDA did not even consider that an ADCOMM was called for that probably should have given us a clear indication of where this one was going.

I also don't expect payers (insurers and Medicare, etc.) to pay for this drug due to it's very marginal efficacy data.

Yes, this does seem to have been the correct call on coverage. CMS somewhat surprisingly apparently wants to maintain its non-coverage CED policy from Aducanumab through to full approval. This will be very difficult for millions of people with Alzheimer’s dementia. A submission for full approval was made the same day as Lecanemab was granted accelerated approval. This could become quite exciting because they might call for an ADCOMM and then we can see all the details about side effects, etc. and have much deeper insight into various aspects of Lecanemab. Without the FDA briefing document the approval process was much much less transparent to me. As an initial guess, it wouldn't be too much information -- it will be more that more information will reveal responders etc.. This will be great!

I have been studying this antibody very extensively over the last few months and I've discussed these results with several AD experts. We all agree: like Adulhelm, the biomarker data looks impressive and unlike Adulhelm, there does appear to be a reduction in cognitive decline at the beginning of dosing.

My take on the cognitive benefit is that Lecanemab is actually quite similar to Aducanumab. On the Aducan thread I have done nearly non-stop regressing and my conclusion is that Aducanumab, Lecanemab and Gantenerumab are all on the same regression parabola. This is somewhat surprising.

Here is the parabolic regression. Aducan was part of the training set. It is truly remarkable how closely Clarity, Graduate 1 & 2 conformed to this prespecified equation. By simply inputting the amount of amyloid removed on PET SUVR one can nearly perfectly determine the cognitive benefit at the group level. This is the basis that the FDA was using for accelerated approval. When the numbers are out by only ~0.02 CDR-sb, it becomes almost impossible to deny that amyloid removal is a valid biomarker. Strangely, amyloid removal as a biomarker then becomes a much stricter restriction than merely hitting a p-value. With the regression it is not good enough to hit any ole p-value; it becomes important to hit a specific p-value that corresponds to the regression line. I have no idea how one could go about setting up the numbers for that.

The PET amyloid SUVR is now thought not to be the actual disease target of interest, though as long as the mabs reduce the down stream beta amyloid as plaques, then an identical cognitive benefit arises. So, the only reason Lecanemab has superior results to Aducanumab and Gantenerumab is because it removes more amyloid. Moving out even marginally to the left on the x-axis to more amyloid clearance gives quadratically improving cognitive benefit.

However, that benefit appears to go away after 6-9 months. After that, with continued repeated dosing there is no difference between the placebo and the drug in reducing cognitive decline.

When I datagrabbed the results from Clarity, I found that the difference between Lecanemab and placebo continued to grow (linearly) right up to the 18th month and likely beyond.

Drag the b slider equation 25 for the vertical and H slider equation 41 for the horizontal slider to see the differences in Clarity. With CDR-sb, the treatment and placebo arms were very very linear. The R^2 in equations 7, 12 and 17 are all nearly 100%. You have a good feeling extrapolating when it is that solid. By eye it is not easy to detect a treatment effect. Yet, when you do a linear regression, the benefit clearly grows through time.

ADAS-cog was less linear, though when you use the centroid of the data using the linear approach you wind up with a 36% benefit which is right in line with other trials have found. Without the linear regression you just have all these jumpy points that seem to have a lot of bounce to them. The headline number that was then reported for Clarity of 26% reduction in decline does not seem as believable or accurate. ADAS-cog is an objective cognitive test so this likely has more forward predictive value than would the CDR-sb which is more retrospective in orientation.
https://www.desmos.com/calculator/haccvoordl The CDR-sb's 27% topline then seems less in tune with the actual benefit in the trial.

This was seen with Aducanumab. Even after years of dosing those on treatment appeared to continue to have a better result relative to placebo. There could be selection involved, though from current evidence it does appear that the benefit continues to increase.

Keep in mind, this also does not stop or reverse cognitive decline, but just reduces it for a brief period.

From the recent phase 2 articles that you referenced I determined the percentile distributions of the different dosing arms. Can't link to the figure directly though it is the Fri Jan 06, 2023 2:02 pm post on the Aducan Celebration thread. The claim that has often been made that treatment does not stop or reverse cognitive decline is not congruent with this evidence. Even 20% of the placebo were stable or improved! For the high dose treatment arm in the phase 2 it was ~40%. Of course, 20% of the placebo improving is not believable; true AD patients do not improve over 18 months, by definition they must decline. However, this is more a problem of how the patients were selected in Clarity. In Trailblazer 2, they used dual tau and amyloid selection and this should amplify the treatment effect signal as it did in Trailblazer (the original). In the most selected group this yielded a 50% reduction in decline on iADRS.
This will be the next news to break when the TB2 completes in April. Moving the ball upfield from 27% reduction in decline to 50% might ruffle some feathers.

The paper with the clinical results is available freely here:


The data I'm referring to is Fig. 9 which shows the cognitive efficacy graphs.

I would paste that data here, but I'm not sure what the rules are about inserting data from anther publication.

The problem here is that we are comparing treated patients with treated patients. What we have seen with Aducanumab is that when we compare the patients who became amyloid negative to those that were still amyloid positive after being treated with Aducan at some point these amyloid positives experience cognitive collapse (i.e., a decline of 4 or more CDR-sb points). None of amyloid negatives exhibited this trajectory. The problem is that AD clinical trials typically only are randomized for 78 weeks. Over the longer term as AD progresses there can be larger cognitive decline that was not seen in the shorter term trials.

Now, you might be thinking: reducing decline for a few months is still great and better than nothing! I agree, however it comes at significant costs.

From my perspective on AD, I feel that Lecanemab represents the end game of dementia in my family. With us, we have experienced cognitive decline that spans decades. It hasn’t been that we did not understand what was happening. It was just there was nothing that could be given as a treatment. Lecanemab is such a relief. I know that within the next few weeks there would be some treatment that could likely be of help to me if I recognized cognitive decline in myself or other family. In our experience even 27% reduction in decline over 30 or 40 years would mean that end stage AD would probably never arise.

This one shows how the longer term benefit could accumulate. Notably here we are only talking about starting dosing at the MCI stage. With us there was at least a decade or two before the MCI stage where there was clear cognitive dysfunction. The potential to bend the curve over such an extended period of time would almost certainly mean that AD would no longer be a force in our life.

The logic involved in going off label if needed, at a micro dose, with extreme safety, minimal cost, and a good chance for positive treatment benefit seems compelling to me. My best estimate is that this would not offer us months of improved quality of life, but probably essentially a functional cure.

First, there have been 3 treatment-related deaths in these trials. All three had to do with patients who had strokes and were given the standard of care for strokes (like blood thinners).

The safety during the randomized portion of Clarity was impressive. There was one fatality due to intracranial hemorrhage during clarity. Specifically, this was a macrohemorrhage that occurred in the placebo arm. In fact there was considerable neuropathology during the core phase of Clarity in the placebo arm. There was substantial ARIA-H microhemorrhages (7.0% of these patients experienced a microhemorrhage). I do not believe is yet widely understood that there is substantial CAA, stroke like events etc. that occur even without mab treatment. The side-effects that are occurring during the trials are not against some pristine background of health. The ARIA etc. that is occurring exactly because none of this existing pathology has ever been treated. These patients are walking around and a range of stroke like risk is simply waiting to be activated.

The response from the drug companies and clinicians is to not use those drugs with anyone who is using Lecanumab. So, if you have a stroke and you're on Lecanumab, you're just out of luck?

Yes, I do agree that this puts everyone in a difficult position. For some patients, there simply might not be a treatment option if they had a stroke and they needed tPA. Clearly that would be a very difficult clinical choice. However, this might not have been true with the Lecanemab patient who had a stroke and then was treated with tPA. In this instance treating with thromboectomy might have been a treatment alternative. The MRIs showed how devastating treating with tPA could be.

I also want safer treatment. With Lecanemab this evolution towards enhanced safety continues. For example, in the Clarity OLE they are now dosing subq. It is possible that when the FDA decides on full approval they might be able to offer a label indication for subq dosing. This would be a great victory for patients if this were possible. Hopefully, now that the finish line is clearly in sight and the funding window for full approval has been opened, that efforts will be redoubled to offer subq.

The second big cost is actually that: the cost. Pricing has not been announced, but since it is an antibody it will be expensive and likely greater than $20K/year.

I am not completely sure about $20k/year. For so many of the people on the sidelines, mab treatment could be decades into the future. They will never pay the patent price. For us, if we were to need early treatment, perhaps even 1 mg/kg treatment a few times per year would be all that we would want. For many patients in such a circumstance mab therapy could largely be an out of pocket payment.

And patients must start taking this years before showing any significant cognitive decline. And we won't even know if those patients will actually ever develop AD.

In our experience all of the family developed it. It wasn’t sporadic. I have full genomes to work with and will be able to use predictive genetics to confirm which of us are at risk. Genome prices might move down to $100 this year. Biogen spent large money on a sequencing project. If genome sequencing were to go mainstream this year at a $100 price point the entire human genome could unlock and then it would be super easy to find which variant was causing our problem. I could then go online and find others with the variant and find out if they were helped by Lecanemab. This would be an amazingly powerful way of fitting the right patient with the right genotype to the right treatment. With logic as strong as that I doubt whether I would even get push back from a doctor.

I am not sure whether such an effort would arise from the corporate side, though it would clearly be an extremely powerful and persuasive argument if one could accurately predict treatment response by specific genotypes. There are many other genotypes aside from APOE epsilon 4 that are likely important for response. If this is all 0.45 CDR-sb, that is one thing. It would be entirely different, if the superresponders could be prospectively identified.

So just start dosing anyone in their 60's or earlier who might have a family history of AD, or maybe displaying earlier MCI for the rest of their lives?

The genetic approach could probably be helpful for others as well. Many of the patients who enroll in AD trials probably do not have extremely strong family histories. Finding those patients that are core AD patients will help to select those who would benefit.

Sounds awesome for Biogen. But that would financially devastate Medicare and insurance companies. So this would dramatically raise health care costs for everyone, for a drug that might slow cognitive decline for a few months? And treat people that we don't know will ever develop AD? I don't think payers will reimburse for that.

The economic argument in favor of Lecanemab treatment for those in the pre stages might become extremely compelling. Consider someone in their 40s earning $80K with children. If that person were to descend into AD over the next 10-15 years they would go from rowing the boat to being a passenger.
The accounting would likely find the cost involved as being large. In our experience the negative externalities are also substantial. Dementing illness becomes like an internal force of destruction of society. Preventative treatment would likely have significant financial paybacks even over the short term. If this all resolves down to money, then at some point those with the sharp pencils might finally realize how massively expensive it is not to treat this. The current hard dollar cost of AD is ~$350 billion and rapidly rising; there are considerable other costs involved that also would eventually translate into real world dollars. My impression is that we have already crossed over to a time that it costs more not to spend more.

I actually understand why the FDA approved this, because they simply look at safety and efficacy and not economics and effects on health care costs. That's not their job. I also like how this has caused excitement in the AD research field which has been so dismal for so long. I'm definitely seeing a lot more interest from investors in this field which we haven't seen for years. So for that, I applaud this effort. But I don't see this as actually doing much to help people I'm afraid.
Last edited by J11 on Mon Jan 09, 2023 11:06 pm, edited 5 times in total.
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Re: Lecanemab approved!

Post by J11 »

circ, thank you I really appreciate comments that recognize when I put words together well. Every once in a while I put in a special effort to reach into my reader's consciousness through the power of words (of course all on a carefully constructed reinforcement schedule so I do not have to strain myself too often. I do wonder what it would be like to be a writer who was playing for all net). I am afraid I am one of those who received a great deal of negative reinforcement about missing commas here and there and not crossing my t's etc.. As a result I was the type whose life goal was to never write a complete sentence in college. {Admittedly, this defeats the entire purpose of education.} This is a big problem in education-- students wind up selecting the subjects they are good at and not the subjects that they are not good at. {Workaround here could be to provide reward marks for students in their weak subjects.} Then you have a society composed of some who communicate with their calculators and others who communicate in words; Becomes somewhat of a communication barrier between the calculator people and the words people. (Please see the Aducan Celebration thread as a reference of repression through regression). With AD mabs, it seems that the calculators won the argument.
Last edited by J11 on Sat Jan 14, 2023 12:57 pm, edited 4 times in total.
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