Secondary Readout.JPG
Celebration Thread! Biogen is going to the FDA with Aducan.
Re: Celebration Thread! Biogen is going to the FDA with Aducan.
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Re: Celebration Thread! Biogen is going to the FDA with Aducan.
This is from page 142 of the CDER report for aducan recently posted onto the FDA site.
This relates to a confusion that arose related to how the statistical analysis plan intended for the high and low dose secondaries to be called. The statistical report from the FDA Briefing document pointed to the high dose secondaries in 302 as being invalidated because the low dose did not achieve statistical significance. Yet, this flow chart apparently shows how the plan wanted the logic flow to occur.
The 302 high dose as seen would unlock the high dose secondaries and the 301 low dose primary as it did not achieve statistical then blocked out the readout on the low dose secondaries. This makes much more sense then having the flow chart read from top line high dose primary to low dose primary to MMSE high dose secondary etc.. As seen above all the high dose secondaries then read out as statistically significant according to the SAP.
It probably would have been best to have had a pre-ADcom meeting to work through these sorts of confusions. As it is this confusion has become an ongoing part of the aducan dialogue, even though it apparently was simply a misinterpretation that did not constructively contribute to the deliberations. I had also been unclear about where the 1 in 10,000 number mentioned in the adcomm originated from; as seen above it was noted in connection with the secondary analysis.
This figure highlights for me once again how the wrong tests were used. It should have been primary iADRS, and secondary order CDR-sb, MMSE (not sure how relevant ADAS-COG and ADCS-ADL would then be as they are contained within iADRS). MMSE is fairly hopeless.
This relates to a confusion that arose related to how the statistical analysis plan intended for the high and low dose secondaries to be called. The statistical report from the FDA Briefing document pointed to the high dose secondaries in 302 as being invalidated because the low dose did not achieve statistical significance. Yet, this flow chart apparently shows how the plan wanted the logic flow to occur.
The 302 high dose as seen would unlock the high dose secondaries and the 301 low dose primary as it did not achieve statistical then blocked out the readout on the low dose secondaries. This makes much more sense then having the flow chart read from top line high dose primary to low dose primary to MMSE high dose secondary etc.. As seen above all the high dose secondaries then read out as statistically significant according to the SAP.
It probably would have been best to have had a pre-ADcom meeting to work through these sorts of confusions. As it is this confusion has become an ongoing part of the aducan dialogue, even though it apparently was simply a misinterpretation that did not constructively contribute to the deliberations. I had also been unclear about where the 1 in 10,000 number mentioned in the adcomm originated from; as seen above it was noted in connection with the secondary analysis.
This figure highlights for me once again how the wrong tests were used. It should have been primary iADRS, and secondary order CDR-sb, MMSE (not sure how relevant ADAS-COG and ADCS-ADL would then be as they are contained within iADRS). MMSE is fairly hopeless.
Re: Celebration Thread! Biogen is going to the FDA with Aducan.
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Re: Celebration Thread! Biogen is going to the FDA with Aducan.
These are from pages 24 and 22 of the CDER report for aducan from the FDA page.
The top figure is of notable interest. Previously on this thread (somewhere?) I pondered how the placebo might actually have a wide range of amyloid levels at the end of the 78 weeks. Yet, this was not overly obvious when looking at the narrow bars placed upon the SUVR values for the placebo in the Briefing Document figures. However, the top figure above does actually show such a dispersion. the vertical line of blue and red circles at 0 Cumulative AUC shows the 301 and 302 placebo. Amusingly and somewhat surprisingly the patient with the lowest measured SUVR at week 78 was not in the high dose 301 study, also not in the high dose 302 study, nor in the 301 low dose or even the 302 low dose, but was in fact in the 301 placebo.
~11? of the 301 and 302 placebo achieved amyloid negativity at week 78??? Basically, these patients perhaps were making their own aducan (i.e., not in a home lab but their own bodies were possibly making antibodies?). One way of saving $56,000 per year. 8 of them
were in 301 and 3 were in 302. This potentially might explain why some of the placebo had such strong cognitive scores at week 78; they had more SUVR decline than many in the high dose arms. Calling such patients "placebo" would seem a misnomer; they might more accurately be described as endogenous high dose aducan. Even the placebo might show a CDR-sb vs. SUVR relationship. A figure that showed the relationship between CDR-sb and SUVR for all patients (high dose, low dose and placebo) could be instructive.
It would obviously be of considerable importance to find predictors of placebo that would have reduced SUVR. Could these placebo be retrospectively removed? They really are not true placebo when the spontaneously demonstrate the trial objective. Perhaps simply remove the lowest 3 quarters of the placebo who had a negative change in SUVR during the trial. It would be of great interest to know how this amyloid removal might have affected cognition.
I am not entirely sure about the meaning of the bottom figure. How does this figure reconcile with the posted secondary results? These results do not appear to be congruent with the reported secondaries.
The top figure is of notable interest. Previously on this thread (somewhere?) I pondered how the placebo might actually have a wide range of amyloid levels at the end of the 78 weeks. Yet, this was not overly obvious when looking at the narrow bars placed upon the SUVR values for the placebo in the Briefing Document figures. However, the top figure above does actually show such a dispersion. the vertical line of blue and red circles at 0 Cumulative AUC shows the 301 and 302 placebo. Amusingly and somewhat surprisingly the patient with the lowest measured SUVR at week 78 was not in the high dose 301 study, also not in the high dose 302 study, nor in the 301 low dose or even the 302 low dose, but was in fact in the 301 placebo.
~11? of the 301 and 302 placebo achieved amyloid negativity at week 78??? Basically, these patients perhaps were making their own aducan (i.e., not in a home lab but their own bodies were possibly making antibodies?). One way of saving $56,000 per year. 8 of them
were in 301 and 3 were in 302. This potentially might explain why some of the placebo had such strong cognitive scores at week 78; they had more SUVR decline than many in the high dose arms. Calling such patients "placebo" would seem a misnomer; they might more accurately be described as endogenous high dose aducan. Even the placebo might show a CDR-sb vs. SUVR relationship. A figure that showed the relationship between CDR-sb and SUVR for all patients (high dose, low dose and placebo) could be instructive.
It would obviously be of considerable importance to find predictors of placebo that would have reduced SUVR. Could these placebo be retrospectively removed? They really are not true placebo when the spontaneously demonstrate the trial objective. Perhaps simply remove the lowest 3 quarters of the placebo who had a negative change in SUVR during the trial. It would be of great interest to know how this amyloid removal might have affected cognition.
I am not entirely sure about the meaning of the bottom figure. How does this figure reconcile with the posted secondary results? These results do not appear to be congruent with the reported secondaries.
Last edited by J11 on Thu Jul 01, 2021 9:02 pm, edited 1 time in total.
Re: Celebration Thread! Biogen is going to the FDA with Aducan.
One newsy item that I have found of interest is that there apparently could be a few anti-amyloids that could arrive on market much sooner than I had thought possible. One recent article suggested that if one of the late stage treatments were to file soon with the FDA that it could be on the shelves by the first quarter of next year. That's fast! It is at least plausible that three anti-amyloids could be in such a circumstance: donanemab, lecanemab and gantenerumab. The prolonged deliberations of aducan after the futility analysis had me thinking that this was how things were done. Apparently not. File the BLA and then it should be roughly 6 months. Perhaps we have reached the point where it is more about preemptive BLA submission; basic idea is to have the BLA paperwork filed --> go in with proving amyloid is removed and then right around the expected PDUFA have the readout on clinical verification.
In addition to the 3 anti-amyloids there is always Tramiprosate. It has already been through 2 phase 3s; they found the epsilon 4 subset appeared to benefit and now we have another phase 3 launched. Wonder whether a short-cut could be available for that one as well? Would it really be that unreasonable? It is based on a safe known natural product; it has a rate of ARIA of 0%, the clinical results though uneven were large,
During that era of research it does not seem that they had PET amyloid on hand. What they seemed to have done is used epsilon 4 genotype as a quick and cheap work around to amyloid scans. They might only be guessing that 44s benefit the most because they do not have as clean a readout for the 33s and 34s. The 33s only had about 70% amyloid positivity. It is a disappointment that they have not shown more of an interest in PET amyloid imaging for the phase 3 ApolloE4 Trial.
The FDA's silence on amyloid evidence for aducan treatment might relate to how for some patients PET amyloid imaging has minimal information value. With epsilon 44s, it does not appear to be particularly relevant to spend $5,000 on a PET amyloid scan when ~95% of those with AD (Mild/Moderate? in the Alzheon trials?) were amyloid positive. Roughly 90% of 34 with cognitive impairment also are amyloid positive. Using current polygenics perhaps an even more accurate assessment is possible. Tramiprosate, though, challenges the amyloid beta plaque paradigm as it interacts more with oligomer amyloid and has posted strong clinical results in those with 44 genotype.
This new regulatory environment for AD could pressure non-US regulators to get onboard. What happens if there were a whole shelf full of anti-AD drugs in the US, but none approved elsewhere? Medical tourism? Filing of BLAs would also initiate regulatory behavior. For example, perhaps another adcom is now not far off. Oh, yea! Cannot wait. Um, how many adcom members are required for quorum?
The regulatory disclosures that might be made in order to gain marketing authorization by such products might make the phase IV trial for aducan somewhat moot. As was noted on thread previously, with amyloid and tau selection statistically significant results with even a short and small trial could be achieved within months. The shelf life for continuing to argue about anti-amyloids is now fairly limited.
In addition to the 3 anti-amyloids there is always Tramiprosate. It has already been through 2 phase 3s; they found the epsilon 4 subset appeared to benefit and now we have another phase 3 launched. Wonder whether a short-cut could be available for that one as well? Would it really be that unreasonable? It is based on a safe known natural product; it has a rate of ARIA of 0%, the clinical results though uneven were large,
During that era of research it does not seem that they had PET amyloid on hand. What they seemed to have done is used epsilon 4 genotype as a quick and cheap work around to amyloid scans. They might only be guessing that 44s benefit the most because they do not have as clean a readout for the 33s and 34s. The 33s only had about 70% amyloid positivity. It is a disappointment that they have not shown more of an interest in PET amyloid imaging for the phase 3 ApolloE4 Trial.
The FDA's silence on amyloid evidence for aducan treatment might relate to how for some patients PET amyloid imaging has minimal information value. With epsilon 44s, it does not appear to be particularly relevant to spend $5,000 on a PET amyloid scan when ~95% of those with AD (Mild/Moderate? in the Alzheon trials?) were amyloid positive. Roughly 90% of 34 with cognitive impairment also are amyloid positive. Using current polygenics perhaps an even more accurate assessment is possible. Tramiprosate, though, challenges the amyloid beta plaque paradigm as it interacts more with oligomer amyloid and has posted strong clinical results in those with 44 genotype.
This new regulatory environment for AD could pressure non-US regulators to get onboard. What happens if there were a whole shelf full of anti-AD drugs in the US, but none approved elsewhere? Medical tourism? Filing of BLAs would also initiate regulatory behavior. For example, perhaps another adcom is now not far off. Oh, yea! Cannot wait. Um, how many adcom members are required for quorum?
The regulatory disclosures that might be made in order to gain marketing authorization by such products might make the phase IV trial for aducan somewhat moot. As was noted on thread previously, with amyloid and tau selection statistically significant results with even a short and small trial could be achieved within months. The shelf life for continuing to argue about anti-amyloids is now fairly limited.
Re: Celebration Thread! Biogen is going to the FDA with Aducan.
It's likely that article, at least for Lecanemab (BAN2401) is about a year premature. Here's the news release from EISAI & Biogen. Note the Sept. 2022 completion of the tightly focused CLARITY trial, which combines an Open-Label Extension trial of people who were on BAN2401 in the previous "201" study to follow them for up to 45 months total, with a new group (split between placebo and a group receiving BAN2401 for 18 months. All groups have a biweekly IV infusion.J11 wrote:... One recent article suggested that if one of the late stage treatments were to file soon with the FDA that it could be on the shelves by the first quarter of next year. That's fast! It is at least plausible that three anti-amyloids could be in such a circumstance: donanemab, lecanemab and gantenerumab. ... Perhaps we have reached the point where it is more about preemptive BLA submission; basic idea is to have the BLA paperwork filed --> go in with proving amyloid is removed and then right around the expected PDUFA have the readout on clinical verification.
In addition to the 3 anti-amyloids there is always Tramiprosate. It has already been through 2 phase 3s; they found the epsilon 4 subset appeared to benefit and now we have another phase 3 launched. Wonder whether a short-cut could be available for that one as well? Would it really be that unreasonable? It is based on a safe known natural product; it has a rate of ARIA of 0%, the clinical results though uneven were large,...
Can't find the source today, but saw that a business article quoting sources that the company has predicted submission by the end of fiscal 2022 (which ends in March 2023-govt. calendars!) for FDA approval. That suggests approval no earlier than mid 2023.Breakthrough Therapy designation is an FDA program intended to expedite the development and review of medicines for serious or life-threatening conditions. The benefits of a Breakthrough Therapy designation include more intensive guidance on an efficient development program as well as eligibility for rolling review and potentially priority review.
The FDA’s Breakthrough Therapy designation for lecanemab is based on the recently published results of a Phase 2b clinical trial (Study 201) of 856 patients with mild cognitive impairment (MCI) due to AD and mild AD with confirmed presence of amyloid pathology.1 The proof-of-concept Study 201 explored the impact of treatment with lecanemab on reducing brain amyloid beta (Aβ) and clinical decline. In this study, pre-specified analysis showed consistent reduction of clinical decline across several clinical and biomarker endpoints at the highest doses.
In March 2021 Eisai and Biogen completed enrollment of 1,795 patients with early AD in the the Phase 3 Clarity AD study. The study’s primary endpoint is expected to be completed by the end of September 2022.
FWIW, I saw a recent talk by biostatistician Dr. Laurel Beckett of UC Davis titled: "A Statistician Reads Alzheimer’s Disease Literature and Attends AAIC" (referring to the upcoming Alz. Assoc conference) in which she emphasized the importance of adhering to pre-specified primary outcomes for both clinical and biomarker effects. So far, it seems that BAN2401 has done that, and the 18-month timelines of CLARITY, which data for 45 months from. subset to look at continued benefit, sounds promising.
Like you, I am hoping that ALZ-801 gets accelerated funding for their planned study in preclinical amyloid positive/cognitively normal ApoE 4/4s. they hope to go to the FDA in 2024, according to this press release: https://www.businesswire.com/news/home/ ... ent-Summit
4/4 and still an optimist!
Re: Celebration Thread! Biogen is going to the FDA with Aducan.
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Re: Celebration Thread! Biogen is going to the FDA with Aducan.
NF52, thank you for your post.
I think the driver for early filing here is with dona. The company is suggesting that they are ready to file sometime later (late?) this year.
That certainly could make things interesting. The potential to develop substantial counter-momentum for anti-amyloids could be checked by the forthcoming disclosure of efficacy for other drugs in the class including donanemab.
The first slide shows the powerful amyloid lowering effects of dona. Remarkably after 24 weeks of treatment the average treated patient lost 68 centiloids; 40% were then amyloid negative. This is the biomarker that the FDA has established in AD. dona massively reduces brain amyloid fast. With aducan it appears to not be quite as rapid. By 26 weeks low and high dose aducan removed ~ 0.075 SUVR. I am not entirely sure about the conversion to centiloid scale though patients started off with ~100 centiloids and removed ~75
centiloid by week 78 and about 1 quarter was removed by week 26 -- ~15 centiloid by week 26?
Nevertheless dona removes an enormous amount of amyloid quickly. Perhaps file early on this finding alone? The phase 3 trial has already been enrolling for a year; give it a few more months and then file; and another 26 weeks for FDA deliberation. That should about definitively establish the profound amyloid lowering effects of dona.
Next there is the link to slowing cognitive decline (bottom figure above). The phase 2 trial cleanly read out a topline significant primary ( p=0.04). They wisely chose iADRS (CDR-sb missed). iADRS seems like a better test; it includes more test content so can average out the fluctuations better. This result was achieved with only ~90 in the treatment and ~90 in the placebo arms with a 32% slowing of decline and a 3.18 absolute difference. Statistically significant results were also achieved at week 36, week 52, and week 64. All of these previous weeks had lower p-values than at 78 weeks. This certainly suggests that statistical significance might be called earlier than the full 78 weeks.
What is even more remarkable is the middle figure above. By selecting on tau apparently the clinical gain widens out to 50% reduction in decline (4.15 points iADRS). At the 36 week time point a statistically significant results was posted even with only ~30 patients in the treatment arm and ~30 in the placebo arm. This result was merely the reported value without reference to covariates such as APOE status or MCI/ Mild AD, etc.. This certainly suggests to me that as was noted months ago on thread a new era of AD clinical trials has arrived with tau imaging. Selecting on tau would allow for small and short trials while achieving needed statistical significance. For whatever reason, the mainstream conversation continues to assume that years and years are needed to prove clinical efficacy of anti-amyloids. From my understanding this is no longer true: compelling results could now be obtained in months.
All of which would rain on the parade on those opposed to anti-amyloids. With dona, very strong evidence in favor of its efficacy has probably already been obtained. 100 patients in the dona arm over 52 weeks might even be enough. Enrollment in the phase 3 has already been ongoing for over a year now.
Given the above, filing early- even this year - would not seem entirely unreasonable. Possibly the only grumbling will be not with amyloid lowering or not even with clinical effectiveness but the accumulated patient experience with the drug. Perhaps this could be worked around by simply increasing the phase 3 by 1,000 patients under the understanding that the readout would occur before full enrollment occurred. With these additional patients possibly interesting further research could be performed. For example, dona has ARIA rates roughly similar to aducan: trying out a different titration scheme to reduce this ARIA might be considered. Also after amyloid negativity is reached and dona treatment is stopped, it would be interesting to see how treatment with aducan might add benefit.
Yet, the main point of interest is that the filing for dona could happen this year. The race for the finish line is on. Other anti-amyloids might then feel it necessary to also step up the pace. For example, lecanemab might then seek an earlier path to market. Lecanemab is a clearly better product than aducan; it has much much less ARIA and it appears to have somewhat stronger efficacy. The phase 2 result demonstrated strong results especially in the mild ADs and APOE+. Perhaps the phase 3 trial and the regulatory process can work in parallel. Tau imaging could also help to find the responders. Regulators from other nations might also see the logic and could choose to leap frog the first generation anti-amyloids and go directly to the second generation with early approvals.
I think the driver for early filing here is with dona. The company is suggesting that they are ready to file sometime later (late?) this year.
That certainly could make things interesting. The potential to develop substantial counter-momentum for anti-amyloids could be checked by the forthcoming disclosure of efficacy for other drugs in the class including donanemab.
The first slide shows the powerful amyloid lowering effects of dona. Remarkably after 24 weeks of treatment the average treated patient lost 68 centiloids; 40% were then amyloid negative. This is the biomarker that the FDA has established in AD. dona massively reduces brain amyloid fast. With aducan it appears to not be quite as rapid. By 26 weeks low and high dose aducan removed ~ 0.075 SUVR. I am not entirely sure about the conversion to centiloid scale though patients started off with ~100 centiloids and removed ~75
centiloid by week 78 and about 1 quarter was removed by week 26 -- ~15 centiloid by week 26?
Nevertheless dona removes an enormous amount of amyloid quickly. Perhaps file early on this finding alone? The phase 3 trial has already been enrolling for a year; give it a few more months and then file; and another 26 weeks for FDA deliberation. That should about definitively establish the profound amyloid lowering effects of dona.
Next there is the link to slowing cognitive decline (bottom figure above). The phase 2 trial cleanly read out a topline significant primary ( p=0.04). They wisely chose iADRS (CDR-sb missed). iADRS seems like a better test; it includes more test content so can average out the fluctuations better. This result was achieved with only ~90 in the treatment and ~90 in the placebo arms with a 32% slowing of decline and a 3.18 absolute difference. Statistically significant results were also achieved at week 36, week 52, and week 64. All of these previous weeks had lower p-values than at 78 weeks. This certainly suggests that statistical significance might be called earlier than the full 78 weeks.
What is even more remarkable is the middle figure above. By selecting on tau apparently the clinical gain widens out to 50% reduction in decline (4.15 points iADRS). At the 36 week time point a statistically significant results was posted even with only ~30 patients in the treatment arm and ~30 in the placebo arm. This result was merely the reported value without reference to covariates such as APOE status or MCI/ Mild AD, etc.. This certainly suggests to me that as was noted months ago on thread a new era of AD clinical trials has arrived with tau imaging. Selecting on tau would allow for small and short trials while achieving needed statistical significance. For whatever reason, the mainstream conversation continues to assume that years and years are needed to prove clinical efficacy of anti-amyloids. From my understanding this is no longer true: compelling results could now be obtained in months.
All of which would rain on the parade on those opposed to anti-amyloids. With dona, very strong evidence in favor of its efficacy has probably already been obtained. 100 patients in the dona arm over 52 weeks might even be enough. Enrollment in the phase 3 has already been ongoing for over a year now.
Given the above, filing early- even this year - would not seem entirely unreasonable. Possibly the only grumbling will be not with amyloid lowering or not even with clinical effectiveness but the accumulated patient experience with the drug. Perhaps this could be worked around by simply increasing the phase 3 by 1,000 patients under the understanding that the readout would occur before full enrollment occurred. With these additional patients possibly interesting further research could be performed. For example, dona has ARIA rates roughly similar to aducan: trying out a different titration scheme to reduce this ARIA might be considered. Also after amyloid negativity is reached and dona treatment is stopped, it would be interesting to see how treatment with aducan might add benefit.
Yet, the main point of interest is that the filing for dona could happen this year. The race for the finish line is on. Other anti-amyloids might then feel it necessary to also step up the pace. For example, lecanemab might then seek an earlier path to market. Lecanemab is a clearly better product than aducan; it has much much less ARIA and it appears to have somewhat stronger efficacy. The phase 2 result demonstrated strong results especially in the mild ADs and APOE+. Perhaps the phase 3 trial and the regulatory process can work in parallel. Tau imaging could also help to find the responders. Regulators from other nations might also see the logic and could choose to leap frog the first generation anti-amyloids and go directly to the second generation with early approvals.
Last edited by J11 on Sat Jul 03, 2021 2:18 am, edited 1 time in total.
Re: Celebration Thread! Biogen is going to the FDA with Aducan.
https://www.alzforum.org/alzbiomarker/ad-vs-ctrl
https://www.alzforum.org/alzbiomarker/cross-disease
alzforum has recently posted a new feature that looks at various biomarkers for AD. This would seem to be a powerful feature in assessing neurodegenerative illness. Now that we are in the era of AD biomarkers this could be quite handy.
Here is the entry for control versus AD for amyloid beta. Effect size of 1.818, z score of 34.3 and a p-value too small to measure; N= 10272 and N=13,930. Facts surely do ruin many fine and enjoyable arguments.
CTRL vs AD: Aβ42 (CSF) 1.818 z = 34.3 | p <0.0001 202 CTRL N=10272, AD N=13930
Rats! the dreaded tau did even better!
CTRL vs AD: tau-total (CSF) 0.402 z = 39.39 | p <0.0001 227 CTRL N=11056, AD N=15441
Here is the comparison for AD versus MCI-stable
MCI-AD vs MCI-Stable: tau-total (CSF) 1.754 z = 18.74 | p <0.0001 28 MCI-AD N=951, MCI-Stable N=1462
This database could be of tremendous therapeutic value. You hear of patients who go to their doctor with a vague complaint about neurological symptoms and then are dragged into a multi-year diagnostic Odyssey to try and sort it all out. These biomakers could be a valuable asset in figuring out such diagnoses efficiently. This could be especially helpful for those who do not live close to specialist medical centers.
For some odd reason alzforum makes no reference to this resource on their main page. J11 will reveal the truth to my readers!
https://www.alzforum.org/alzbiomarker
https://www.alzforum.org/alzbiomarker/cross-disease
alzforum has recently posted a new feature that looks at various biomarkers for AD. This would seem to be a powerful feature in assessing neurodegenerative illness. Now that we are in the era of AD biomarkers this could be quite handy.
Here is the entry for control versus AD for amyloid beta. Effect size of 1.818, z score of 34.3 and a p-value too small to measure; N= 10272 and N=13,930. Facts surely do ruin many fine and enjoyable arguments.
CTRL vs AD: Aβ42 (CSF) 1.818 z = 34.3 | p <0.0001 202 CTRL N=10272, AD N=13930
Rats! the dreaded tau did even better!
CTRL vs AD: tau-total (CSF) 0.402 z = 39.39 | p <0.0001 227 CTRL N=11056, AD N=15441
Here is the comparison for AD versus MCI-stable
MCI-AD vs MCI-Stable: tau-total (CSF) 1.754 z = 18.74 | p <0.0001 28 MCI-AD N=951, MCI-Stable N=1462
This database could be of tremendous therapeutic value. You hear of patients who go to their doctor with a vague complaint about neurological symptoms and then are dragged into a multi-year diagnostic Odyssey to try and sort it all out. These biomakers could be a valuable asset in figuring out such diagnoses efficiently. This could be especially helpful for those who do not live close to specialist medical centers.
For some odd reason alzforum makes no reference to this resource on their main page. J11 will reveal the truth to my readers!
https://www.alzforum.org/alzbiomarker
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Re: Celebration Thread! Biogen is going to the FDA with Aducan.
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